In the electrodeposition of metals, a widely used industrial technique, bubbles of gas generated near the cathode can adversely affect the quality of the metal coating. Here we use phase-contrast radiology with synchrotron radiation to witness directly and in real time the accumulation of zinc on hydrogen bubbles. This process explains the origin of the bubble-shaped defects that are common in electrodeposited coatings.

We have demonstrated an improvement of photovoltaic performance based on the nanostructured ZnO/poly(3-hexylthiophene) (P3HT) hybrid through interface molecular modification on ZnO nanorod surface. By probing the carrier dynamics at ZnO/P3HT interfaces, we have found that the interfacial molecules can play the role of assisting charge separation and suppression of back recombination at interfaces, which accounts for the observed enhanced short circuit current (Jsc) and open circuit voltage (Voc) in photovoltaic performance.

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IL-19, a proinflammatory cytokine, belongs to the IL-10 family. IL-19 is induced in systemic inflammatory response syndrome, but its pathophysiological function in sepsis is unclear. Our aim was to determine the roles of IL-19 in endotoxin-induced tissue damage in vivo and in vitro. We examined serum levels of IL-19 in sepsis patients and healthy volunteers, determined the in vitro effects of IL-19 on lung epithelial cells, liver cells, and neutrophils, and analyzed the tissue expression of IL-19 and its receptors in murine endotoxic shock. Electroporation-mediated gene transfer of mouse IL-19-soluble receptor plasmid DNA was used to determine the effects of IL-19 depletion in preventing endotoxic shock-induced tissue damage in mice. We found that serum levels of IL-19 were higher in patients than in healthy volunteers (n = 28, P = 0.001). IL-19 induced apoptosis in lung epithelial cells and reactive oxygen species production in liver cells in vitro. IL-19 also promoted neutrophil chemotaxis, reduced neutrophil apoptosis, and induced the production of proinflammatory cytokines and chemokines (IL-1[beta], IL-6, IL-8, CCL5, and CXCL9) in lung epithelial cells. In LPS-challenged mice, transcripts of IL-19 and its receptors were up-regulated in heart, lung, liver, and kidney tissue. Neutrophil infiltration in lung and liver tissue, and serum levels of alanine transaminase and aspartate transaminase, were lower in mice electroporated with IL-19-soluble receptor plasmid DNA before LPS treatment compared with control mice. These results suggest that up-regulated IL-19 may be involved in lung and liver tissue injury in murine endotoxic shock.