Experimental evaluation into novel, low cost, modular PEMFC stack

Attribution-NonCommercial-NoDerivs 3.0 Unported (CC BY-NC-ND 3.0)The Polymer Electrolyte Membrane Fuel Cell (PEMFC), despite being regarded as an ideal replacement to the internal combustion engine, is still not an economically attractive pri-mover due to a number of key challenges that have yet to be fully resolved; some of which include degradation to cell components resulting in inadequate lifetimes, specialised and costly manufacturing processes and poor gravimetric/volumetric energy densities. This paper presents a novel stack concept which removes the conventional bi polar plate (BPP), a component that is responsible for up to 80% of total stack weight and 90+% of stack volume in some designs. The removal of said component not only improves the volumetric and gravimetric energy density of the PEMFC stack but drastically reduces the cost of the stack by removing all costly manufacturing processes associated with PEMFC component machining while the functionality of the traditional BPP is still retained by the unique stack design. The stack architecture is first presented and then the characterisation of the PEMFC is shown over a wide range of operating scenarios. The experimental studies suggest that the performance of the new design is comparable to that of traditional stacks but at significantly less cost price.Final Published versio

Genetic variants in <i>TNF</i><b>α</b>, <i>TGFB1, PTGS1</i> and <i>PTGS2</i> genes are associated with diisocyanate-induced asthma

<div><p></p><p>Diisocyanates are the most common cause of occupational asthma, but risk factors are not well defined. A case-control study was conducted to investigate whether genetic variants in inflammatory response genes (<i>TNFα, IL1α, IL1β, IL1RN, IL10, TGFB1, ADAM33, ALOX-5, PTGS1, PTGS2</i> and <i>NAG-1/GDF15</i>) are associated with increased susceptibility to diisocyanate asthma (DA). These genes were selected based on their role in asthmatic inflammatory processes and previously reported associations with asthma phenotypes. The main study population consisted of 237 Caucasian French Canadians from among a larger sample of 280 diisocyanate-exposed workers in two groups: workers with specific inhalation challenge (SIC) confirmed DA (DA⁺, <i>n</i> = 95) and asymptomatic exposed workers (AW, <i>n</i> = 142). Genotyping was performed on genomic DNA, using a 5′ nuclease PCR assay. After adjusting for potentially confounding variables of age, smoking status and duration of exposure, the <i>PTGS1</i> rs5788 and <i>TGFB1</i> rs1800469 single nucleotide polymorphisms (SNP) showed a protective effect under a dominant model (OR = 0.38; 95% CI = 0.17, 0.89 and OR = 0.38; 95% CI = 0.18, 0.74, respectively) while the <i>TNFα</i> rs1800629 SNP was associated with an increased risk of DA (OR = 2.08; 95% CI = 1.03, 4.17). Additionally, the <i>PTGS2</i> rs20417 variant showed an association with increased risk of DA in a recessive genetic model (OR = 6.40; 95% CI = 1.06, 38.75). These results suggest that genetic variations in <i>TNFα, TGFB1, PTGS1</i> and <i>PTGS2</i> genes contribute to DA susceptibility.</p></div