The photoactive materials in dye‐sensitized solar cells (DSSCs) are conventionally produced by colloid coating and heat treatment followed by dye adsorption by dipping in solution. One disadvantage of this procedure is that only heat‐resistant materials can be used. Here the one‐step self‐assembly of ZnO/eosin Y thin films is reported. It is shown that a large proportion of the incorporated eosin Y dye molecules act as sensitizers, making the films suitable as sensitized photoelectrodes in DSSCs. No heat treatment is required, allowing non‐heat‐resistant substrates such as flexible conductive plastic films to be used.
Properties of ionic currents in smooth muscle membranes of the longitudinal muscle layer of the rabbit ileum were investigated using the single electrode voltage clamp method. In the present experiments, this method was applicable only to the smooth muscle ball (fragment) and not for the dispersed whole cell, because of incompleteness of the voltage clamping. A voltage step elicited a transient inward current followed by an outward current. This outward current was partly inhibited by Mn2+ or nisoldipine or by a reduction in the extracellular [Ca2+] ([Ca2+]o). Tetraethylammonium (TEA) reduced the delayed outward current in a dose-dependent manner, but 50 mM TEA did not produce a complete block of a residual current. When the pipette contained K+-free (Cs+ with TEA+) solution, the residual outward current was abolished. The inward current was elicited at -30 mV (holding potential of -60 mV) and reached the maximal value at +10 mV; the polarity was reversed at +60 mV. This inward current depended on the [Ca2+]o and was blocked by Mn2+ or nisoldipine. Ba2+ also permeated the membrane, and the inward current evoked by Ba2+ was also blocked by Mn2+ or nisoldipine. Reduction of [Na+]o in a solution containing 2.4 mM Ca2+ neither modified the current-voltage relation nor the decay of the inward current, but when [Ca2+]o was reduced to below 1 microM, Na+ permeated the membrane and was blocked by nisoldipine. In conclusion, ionic currents were recordable from the fragmented ball of the longitudinal muscle of rabbit ileum. There were at least two K+ currents as the outward current (Ca2+-dependent K+ and delayed K+ currents) and a Ca2+ current as the inward current. The property of the Ca2+ channel was similar to that observed with other preparations.
Cathepsin B (CB) is a cysteine lysosomal protease implicated in a number of inflammatory diseases. Although it is now evident that caspase-1, an essential enzyme for maturation of interleukin-1beta (IL-1beta), can be activated through the inflammasome, there is still evidence suggesting the existence of lysosomal-proinflammatory caspase pathways. In the present study, a marked induction of pro-IL-1beta, its processing to the mature form and secretion were observed in the primary cultured microglia prepared from wild-type mice after stimulation with chromogranin A (CGA). Although pro-IL-1beta also markedly increased in microglia prepared from CB-deficient mice, CB-deficiency abrogated the pro-IL-1beta processing. CA-074Me, a specific inhibitor for CB, inhibited the pro-IL-1beta maturation and its release from microglia. Furthermore, the caspase-1 activation was also inhibited by CA-074Me and E-64d, a broad cysteine protease inhibitor. After treatment with CGA, CB was markedly induced at both protein and mRNA levels. The induced pro-CB was rapidly processed to its mature form. The immunoreactivity for CB co-localized with both that for caspase-1 and the cleaved IL-1beta, in the acidic enlarged lysosomes. Inconsistent with these in vitro observations, the immunoreactivity for the cleaved IL-1beta was markedly observed in microglia of the hippocampus from aged wild-type but not CB-deficient mice. These observations strongly suggest that CB plays a key role in the pro-IL-1beta maturation through the caspase-1 activation in enlarged lysosomes of CGA-treated microglia. Therefore, either pharmacological or genetic inhibition of CB may provide therapeutic intervention in inflammation-associated neurological diseases.
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