A sol−gel process is described to produce phosphoric acid (PA)-doped polybenzimidazole (PBI) films that operate as fuel cell membranes above 150 °C for extended periods of time without the need for feed gas humidification. When solutions of high molecular weight heterocylic polymers such as polybenzimidazoles in polyphosphoric acid (PPA) were cast into films, a transition from solution state to gel state was observed during the hydrolysis of the solvent from PPA (a good solvent for PBI) to PA (a poor solvent for PBI). The resulting membranes retained high levels of phosphoric acid in the gel structure and exhibited high ionic conductivities and stable mechanical properties at elevated temperatures. Preliminary fuel cell tests have demonstrated the feasibility of such PBI membranes from the sol−gel process for operating a fuel cell at temperatures above 150 °C without any feed gas humidification or pressure requirements for more than 1000 h.

Long‐term durability testing of polybenzimidazole (PBI)‐based polymer electrolyte membrane (PEM) fuel cells was performed using test protocols designed to simulate fuel cell operational situations which may be found in real applications. The fuel cell voltages and phosphoric acid (PA) loss were carefully monitored over thousands of hours and hundreds of cycles. In the typical operating range for high temperature PEM fuel cells (160 °C), the fuel cell voltage degradation rate was 4.9 μV h–1 for steady‐state operation. The PA loss rates were generally low and indicated that long‐term operation (>10,000 h) was possible without significant performance degradation due to PA loss from the membrane. Dynamic durability tests also showed that the PA loss rate from the membrane electrode assemblies (MEAs) depended on cell operating temperature and load conditions. Under all conditions, the PA loss was a relatively small amount of the total PA in the membrane.

A series of polybenzimidazoles (PBIs) incorporating main chain pyridine groups were synthesized from the pyridine dicarboxylic acids (2,4‐, 2,5‐, 2,6‐ and 3,5‐) and 3,3′,4,4′‐tetraaminobiphenyl, using polyphosphoric acid (PPA) as both solvent and polycondensation reagent. A novel process, termed the PPA process, has been developed to prepare phosphoric acid (PA) doped PBI membranes by direct‐casting of the PPA polymerization solution without isolation or re‐dissolution of the polymers. The subsequent hydrolysis of PPA to PA by moisture absorbed from the atmosphere usually induced a transition from the solution state to a gel‐like state and produced PA‐doped PBI membranes with a desirable suite of physiochemical properties. The polymer structure characterization included inherent viscosity (I.V.) determination as a measurement of polymer molecular weight and thermal stability assessment via thermogravimetric analysis. Physiochemical properties of the doped membrane were studied by measurements of the PA doping level, ionic conductivity and mechanical properties. The resulting pyridine‐based polybenzimidazole membranes displayed high PA doping levels, ranging from 15 to 25 mol of PA per PBI repeat unit, which contributed to their unprecedented high proton conductivities of 0.1 to 0.2 S cm–1 at 160 °C. The mechanical property measurements showed that the pyridine‐based PBI membranes were thermally stable and maintained mechanical integrity even at high PA doping levels. Preliminary fuel cell tests demonstrated the feasibility of the novel pyridine‐based PBI (PPBI) membranes from the PPA process for operating fuel cells at temperatures in excess of 120 °C without any external humidification.

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Mass-transport studies of phosphoric acid ͑PA͒-doped meta-polybenzimidazole ͑PBI͒ fuel cell membranes are described. In this study, the fundamental differences in transport properties between m-PBI/PA membranes prepared by conventional imbibing procedures and the polyphosphoric acid ͑PPA͒ process are explored. The membranes were characterized by proton conductivity and multinuclear ͑ 1 H and 31 P͒ magnetic resonance measurements. Both short-range and long-range dynamical processes were investigated by spin-lattice and spin-spin relaxation time measurements and by pulsed field gradient diffusion, respectively. Comparative data for pure PA and PPA are included. The high proton conductivity ͑0.13 S/cm at 160°C͒ of the PPA-processed membranes is correlated with rapid proton self-diffusion ͑3 ϫ 10 −6 cm 2 /s at 180°C͒. The 31 P results reveal the presence of both PA and the dimeric pyrophosphoric acid and indicate strong interaction between the phosphate groups and the m-PBI matrix, with negligible anionic transport for both kinds of membranes. The higher concentration of PA in the PPA-processed membranes and differences in membrane morphology may provide an additional proton-transport mechanism involving rapid exchange between the PA and pyrophosphoric acid species.

Chronic inflammation accompanies obesity and limits subcutaneous white adipose tissue (WAT) expandability, accelerating the development of insulin resistance and type 2 diabetes mellitus. MicroRNAs (miRNAs) influence expression of many metabolic genes in fat cells, but physiological roles in WAT remain poorly characterized. Here, we report that expression of the miRNA in subcutaneous WAT corresponds with insulin sensitivity in obese mice and humans. To examine the hypothesis that restoration of expression in WAT improves insulin sensitivity, we injected adenovirus (Adv) expressing into the subcutaneous fat pad of diabetic mice. Exogenous expression in the subcutaneous WAT depot of obese mice coupled improved insulin sensitivity and increased energy expenditure with decreased ectopic fat deposition in the liver and reduced WAT inflammation. High-throughput proteomic profiling and RNA-Seq suggested that targets the transcription factor STAT1 to limit the actions of the proinflammatory cytokine interferon-γ (IFN-γ) that would otherwise restrict WAT expansion and decrease insulin sensitivity. We further demonstrated that opposes the actions of IFN-γ, suggesting an important role for in defending adipocytes against proinflammatory cytokines that reduce peripheral insulin sensitivity. Together, our data identify a critical molecular signaling axis, elements of which are involved in uncoupling obesity from metabolic dysfunction.

Background/Objectives:Although obesity is associated with low-grade inflammation and metabolic disorders, clinical studies suggested some obese people were metabolically healthy with smaller adipocyte size compared with metabolically abnormal obese (MAO). This indicated adipocyte size may be an important predictor underlay the distinction between MAO and metabolically healthy obese. As recent study has shown that adipocytes expressed class II major histocompatibility complex (MHCII), which functioned as APCs during obesity. However, the relationship between adipocyte hypertrophy and MHCII expression was not involved. Here we hypothesize that hypertrophic adipocytes could be associated with upregulating MHCII to influence adipose tissue metabolism.Methods:Adipocytes were sorted by fluorescence-activated cell sorting (FACS) according to the cell size from MAO mice. The activation of MHCII, T cells and related signaling molecules were examined by FACS, ELISA and western blotting. 3T3-L1 cell line and primary adipocytes were used to examine the effect of free fatty acids (FFA) on adipocytes enlargement and MHCII expression.Results:MAO mice had a significant increase in adipocytes size and FFA concentration. The large adipocytes from both obese and non-obese mice expressed higher levels of MHCII than small adipocytes. Importantly, large adipocytes from obese mice stimulated CD4+ T cells to secrete more interferon (IFN)-γ. Furthermore, the activation of the JNK-STAT1 pathway was involved in upregulation of MHCII in large adipocytes. In vitro FFA treatment promoted adipocyte hypertrophy and expression of MHCII-associated genes.Conclusions:This study demonstrates that large adipocytes highly express MHCII and function as APC to stimulate IFN-γ-expressing CD4+ T cells, in which FFA may have important roles before IFN-γ elevated. These findings suggest that adipocyte hypertrophy, rather than overall obesity, is the major contributor to adipose tissue inflammation and insulin resistance.