We now demonstrate a new class of a polymer proton exchange membrane for fuel cells, capable of combining low cost and high proton conductivity under low humidity conditions. The novel phosphoric acid (PA)-doped sulfonated polyimide (SPI) and polybenzimidazole (PBI) blend membrane enables proton conductivities of approximately 0.5 and 0.1 S cm⁻¹ at 120 °C and 45%RH and at 30 °C and 30%RH, respectively. These conductivities were approximately two orders of magnitude higher than those of Nafion 117 due to a new proton transport pathway between phosphoric acid and sulfonic acid in the blend membrane. In addition, the membrane showed no signs of performance degradation at 120 °C and 0%RH after 1000 hours of operation, and maintained a proton conductivity value of more than 0.01 S cm⁻¹. Consequently, this material shows promise as a novel proton exchange membrane and may have potential applications for use in fuel cells.

Chronic obstructive pulmonary disease (COPD) is a lung disease caused by an inflammatory response to various inhaled toxins, especially cigarette smoke. Reactive oxygen species (ROS) and epigenetic abnormality are intimately related to the pathology of COPD, and the overproduction of ROS results in a decrease of histone deacetylase 2 (HDAC2), leading to glucocorticoid resistance. Therefore, a novel treatment that simultaneously reduces ROS level and glucocorticoid resistance is urgently needed. In this study, we developed a codelivery system using core-shell type lipid-polymer nanoparticles (LPNs) composed of a poly(lactic acid) (PLA) core encapsulating a potent antioxidant Mn-porphyrin dimer (MnPD) and a cationic lipid (DOTAP) shell that binds HDAC2-encoding plasmid DNA (pHDAC2), as a new therapeutic approach toward COPD. The transfection of pHDAC2 combined with the elimination of ROS by MnPD exhibited a significant enhancement of intracellular HDAC2 expression levels, suggesting that the multi-antioxidative activity of MnPD plays a crucial role in the expression of HDAC2. Moreover, treatment with LPNs efficiently ameliorated the steroid resistance in COPD models in vitro as evidenced by the lowered expression levels of IL-8. Recovery from mitochondrial dysfunction may be the mechanism underlying the action of LPNs. The PLA-MnPD/DOTAP/pHDAC2 system proposed offers a new therapeutic approach for COPD based on the synergism of ROS elimination and HDAC2 expression.