Mechanical endurance of polymer electrolyte membrane and PEM fuel cell durability

The life of proton exchange membrane fuel cells (PEMFC) is currently limited by the mechanical endurance of polymer electrolyte membranes and membrane electrode assemblies (MEAs). In this paper, the authors report recent experimental and modeling work toward understanding the mechanisms of delayed mechanical failures of polymer electrolyte membranes and MEAs under relevant PEMFC operating conditions. Mechanical breach of membranes/MEAs in the form of pinholes and tears has been frequently observed after long‐term or accelerated testing of PEMFC cells/stacks. Catastrophic failure of cell/stack due to rapid gas crossover shortly follows the mechanical breach. Ex situ mechanical characterizations were performed on MEAs after being subjected to the accelerated chemical aging and relative humidity (RH) cycling tests. The results showed significant reduction of MEA ductility manifested as drastically reduced strain‐to‐failure of the chemically aged and RH‐cycled MEAs. Postmortem analysis revealed the formation and growth of mechanical defects such as cracks and crazing in the membranes and MEAs. A finite element model was used to estimate stress/strain states of an edge‐constrained MEA under rapid RH variations. Damage metrics for accelerated testing and life prediction of PEMFCs are discussed. © 2006 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 44: 2346–2357, 2006     

Calotropis procera extract induces apoptosis and cell cycle arrest at G2/M phase in human skin melanoma (SK-MEL-2) cells

Calotropis procera (family: Asclepiadaceae) contains cardiac glycosides which are cytotoxic to cancer cells. The extracts of C. procera have been reported to be cytotoxic to many cancer cell lines and this is the first report against the human skin melanoma cells (SK-MEL-2). The SK-MEL-2 cells treated with C. procera methanolic extract (CPME) were analysed for growth inhibition and apoptosis. The exposure of phosphatidylserine in apoptotic SK-MEL-2 was analysed by using the Annexin-V FITC flow cytometry method. In CPME-treated SK-MEL-2 cells, 19.6% of apoptotic and 58.3% dead cells were observed. The 15.97% and 15.85% of early apoptotic cells were found at 20 μg/mL of the ouabain and paclitaxel, respectively. Active caspases, nuclear degradation confirmed apoptotic SK-MEL-2 cells in time- and dose-dependent manner. The cell cycle analysis shows that CPME treated cells halt at G2/M phase. Significant cytotoxic activity of CPME against SK-MEL-2 may be attributed to its high cardenolide content.