A Water-Free ITIES: Ionic Liquid/Oil Interface for Base Metal Nanostructure Formation - Zn Case

Reductive metal deposition at the interface between two immiscible electrolyte solutions (ITIES), the oil/water interface, is an attractive methodology to produce metal nanostructures. However, the metals that can be deposited are limited to noble metals; otherwise, water molecules are reduced. Herein, a method to overcome this limitation by utilizing a novel water-free ITIES between a hydrophilic ionic liquid and oil was introduced. As proof-of-concept experiments, the reductive deposition of zinc, a base metal with a standard redox potential more negative than that of water, was successfully realized at the ionic liquid/oil interface. The morphology of the zinc nanostructures was investigated, and the reaction mechanism was discussed, in which the electron transfer and ion transfer reactions across the interface simultaneously occurred to maintain the electroneutrality of the liquids

Electrochemical liquid-liquid interface between oil and ionic liquid for reductive deposition of metal nanostructures

An electrochemical system at the ionic liquid (IL) | oil (O) interface has been constructed and utilized as electrochemical reaction field for reductive deposition of metal nanostructures. The interface between 1-(3-hydroxypropyl)-3-methylimidazolium chloride (C3OHmimCl), a hydrophilic IL, and 1, 6-dichlorohexane (containing an organic electrolyte) exhibits a polarized potential window of 150 mV, which is limited by the ion transfer (IT) of the IL cation and anion at the positive and negative edges, respectively. The polarizable IL | O interface has allowed to record voltammograms for the electron transfer (ET) and IT processes across the IL | O interface that are involved in the reductive deposition of gold at the IL | O interface. The ET between AuCl₄− in the IL phase and decamethylferrocene in the O phase proceeds without applying external voltage by coupling with the IT of AuCl₄−, spontaneously forming Au nanostructures at the IL | O interface

Reductive deposition of aluminum at a water-free ionic liquid/oil interface

The oil/water interface has been used as a reaction field for interfacial metal deposition via electron transfer between metal ions and reducing agents across the interface. However, the metals that can be deposited at liquid/liquid interfaces are limited to noble metals whose standard redox potential is more positive than that of water. In the present study, we designed a water-free liquid/liquid interface between a hydrophilic ionic liquid (IL) and oil (O) and succeeded in reductively depositing Al, a base metal that has a significantly negative standard redox potential and that is not reduced at water-based liquid/liquid interfaces. The morphology of the deposited Al was investigated and the reaction mechanism was explained as a combination of electron transfer and ion transfer across the IL/O interface

Double deletion of tetraspanins CD9 and CD81 in mice leads to a syndrome resembling accelerated aging

Abstract Chronic obstructive pulmonary disease (COPD) has been recently characterized as a disease of accelerated lung aging, but the mechanism remains unclear. Tetraspanins have emerged as key players in malignancy and inflammatory diseases. Here, we found that CD9/CD81 double knockout (DKO) mice with a COPD-like phenotype progressively developed a syndrome resembling human aging, including cataracts, hair loss, and atrophy of various organs, including thymus, muscle, and testis, resulting in shorter survival than wild-type (WT) mice. Consistent with this, DNA microarray analysis of DKO mouse lungs revealed differential expression of genes involved in cell death, inflammation, and the sirtuin-1 (SIRT1) pathway. Accordingly, expression of SIRT1 was reduced in DKO mouse lungs. Importantly, siRNA knockdown of CD9 and CD81 in lung epithelial cells additively decreased SIRT1 and Foxo3a expression, but reciprocally upregulated the expression of p21 and p53, leading to reduced cell proliferation and elevated apoptosis. Furthermore, deletion of these tetraspanins increased the expression of pro-inflammatory genes and IL-8. Hence, CD9 and CD81 might coordinately prevent senescence and inflammation, partly by maintaining SIRT1 expression. Altogether, CD9/CD81 DKO mice represent a novel model for both COPD and accelerated senescence