Investigation into the characteristics of proton exchange membrane fuel cell-based power system

© The Institution of Engineering and Technology.Fuel cells (FCs) use hydrogen as their prime fuel source, which promotes them as one of the attractive options for clean energy generators. Though they have been around for some time, their characteristics are not yet fully understood. This study offers a thorough investigation into the characteristics of proton exchange membrane (PEM) type of FCs based power system. This study first presents a concise explanation of the working principles of the PEM electrolyser and FCs supported by novel modelling using MATLAB. The simulation results are then validated by a series of experiments carried out on operational 500 mW FC followed by detailed performance parameters of such type of FCs. Parameters affect the efficiencies of each part of the system are investigated and the total system's efficiency is then calculated. The efficiency of the electrolyser and PEM FC was found to be 85 and 60%, respectively. Polarisation curve has been used in order to evaluate FC's performance. From the polarisation curve, it is noted the efficiency of the FC increases with increasing pressure and temperature. The activation losses are reduced when the temperature increased. Moreover, the mass transfer is enhanced toward reducing the PEMFC's resistance

A redox state-dictated signalling pathway deciphers the malignant cell specificity of CD40-mediated apoptosis

CD40, a member of the tumour necrosis factor receptor (TNFR) superfamily, has the capacity to cause extensive apoptosis in carcinoma cells, while sparing normal epithelial cells. Yet, apoptosis is only achieved by membrane-presented CD40 ligand (mCD40L), as soluble receptor agonists are but weakly pro-apoptotic. Here, for the first time we have identified the precise signalling cascade underpinning mCD40L-mediated death as involving sequential TRAF3 stabilisation, ASK1 phosphorylation, MKK4 (but not MKK7) activation and JNK/AP-1 induction, leading to a Bak- and Bax-dependent mitochondrial apoptosis pathway. TRAF3 is central in the activation of the NADPH oxidase (Nox)-2 component p40phox and the elevation of reactive oxygen species (ROS) is essential in apoptosis. Strikingly, CD40 activation resulted in down-regulation of Thioredoxin (Trx)-1 to permit ASK1 activation and apoptosis. Although soluble receptor agonist alone could not induce death, combinatorial treatment incorporating soluble CD40 agonist and pharmacological inhibition of Trx-1 was functionally equivalent to the signal triggered by mCD40L. Finally, we demonstrate using normal, ‘para-malignant’ and tumour-derived cells that progression to malignant transformation is associated with increase in oxidative stress in epithelial cells, which coincides with increased susceptibility to CD40 killing, while in normal cells CD40 signalling is cytoprotective. Our studies have revealed the molecular nature of the tumour specificity of CD40 signalling and explained the differences in pro-apoptotic potential between soluble and membrane-bound CD40 agonists. Equally importantly, by exploiting a unique epithelial culture system that allowed us to monitor alterations in the redox-state of epithelial cells at different stages of malignant transformation, our study reveals how pro-apoptotic signals can elevate ROS past a previously hypothesised ‘lethal pro-apoptotic threshold’ to induce death; an observation that is both of fundamental importance and carries implications for cancer therap