Membrane and Electrode Materials for Alkaline Membrane Fuel Cells

This paper and the associated presentation will describe the latest developments regarding alkaline anion exchange membrane (AAEM) fuel cells at Surrey. The program of work conducted has been targeted at the materials development of both membranes and electrodes containing alkaline ionomers and as such has focused on H-2/O-2 fuel cell testing. Radiation-grafted AAEMs can be made with fully hydrated thicknesses between 18 - 80 mu m with conductivities in water of up to 0.06 S cm(-2) at 60 degrees C. A peak power density of 230 mW cm(geo)(-2) and a maximum current density at full discharge of 1.3 A cm(geo)(-2) have been obtained in a H-2/O-2 fuel cell at 50 degrees C with a 18 mu m AAEM and Toray carbon paper based electrodes (Pt/C(20%mass), 0.5 mg(pt) cm(geo)(-2) loading) that were treated with Surrey's first generation alkaline ionomer. A future priority is the development of the next generation alkaline ionomer

Membrane and Electrode Materials for Alkaline Membrane Fuel Cells

This paper and the associated presentation will describe the latest developments regarding alkaline anion exchange membrane (AAEM) fuel cells at Surrey. The program of work conducted has been targeted at the materials development of both membranes and electrodes containing alkaline ionomers and as such has focused on H-2/O-2 fuel cell testing. Radiation-grafted AAEMs can be made with fully hydrated thicknesses between 18 - 80 mu m with conductivities in water of up to 0.06 S cm(-2) at 60 degrees C. A peak power density of 230 mW cm(geo)(-2) and a maximum current density at full discharge of 1.3 A cm(geo)(-2) have been obtained in a H-2/O-2 fuel cell at 50 degrees C with a 18 mu m AAEM and Toray carbon paper based electrodes (Pt/C(20%mass), 0.5 mg(pt) cm(geo)(-2) loading) that were treated with Surrey's first generation alkaline ionomer. A future priority is the development of the next generation alkaline ionomer

A Disintegrin and Metalloproteinase Protein 8 (ADAM 8) in Autism Spectrum Disorder: Links to Neuroinflammation

Laila Al-Ayadhi,1,2 Amani Abualnaja,3 Abdullah AlZarroug,3 Turki Alharbi,3 Abdulrahman M Alhowikan,1,2 Dost M Halepoto,1 Sarah Al-Mazidi4 1Autism Research and Treatment Centre, Faculty of Medicine, King Saud University, Riyadh, 11461, Saudi Arabia; 2Department of Physiology, Faculty of Medicine, King Saud University, Riyadh, 11461, Saudi Arabia; 3College of Medicine, Imam Mohammad Ibn Saud Islamic University, Riyadh, 11432, Saudi Arabia; 4College of Medicine, Department of Physiology, Imam Mohammad Ibn Saud Islamic University, Riyadh, 11432, Saudi ArabiaCorrespondence: Sarah Al-Mazidi, College of Medicine, Department of Physiology, Imam Mohammad Ibn Saud Islamic University, P.O Box: 5701, Riyadh, 11432, Saudi Arabia, Tel +966-553-007-441, Email [email protected]: Converging lines of evidence confirmed neuroinflammation’s role in autism spectrum disorder (ASD) etiological pathway. A disintegrin and metalloproteinase 8 (ADAM8) play major roles in inflammatory and allergic processes in various diseases.Aim: This study aimed to investigate ADAM8 plasma levels in autistic children compared to healthy controls. Also, to discover the association between ADAM8, disease severity, and neuroinflammation in ASD.Methodology: This case–control study included children with ASD (n=40) and aged-matched healthy controls (n=40). The plasma levels of the ADAM 8 were determined using enzyme-linked immunosorbent assay (ELISA). The assessment of ASD severity and social and sensory behaviors were categorized as mild, moderate and severe. Correlations among ADAM8 plasma levels and ASD severity scores [Childhood Autism Rating Scale (CARS), Social Responsiveness Scale (SRS) and Short Sensory Profile (SSP)] were obtained by Spearman correlation coefficient (r).Results: ASD children (n=40), including severe autism (n=21) and mild-to-moderate autism (n=19), showed significantly (p ≤ 0.05) lower plasma levels of ADAM8 [4683 (2885– 5229); 4663 (4060– 5000); 4632 (2885– 5229)], respectively, than those of healthy controls [5000 (4047– 5000)] [median (IQR) pg/mL]. However, there was no significant difference between the ADAM8 levels of children with severe and mild-to-moderate autism (p = 0.71). Moreover, ADAM8 plasma levels were not significantly correlated with the severity of ASD measured by behavioral scales [CARS (r= − 0.11, p=0.55), SRS (r=0.11, p= 0.95), SSP (r=− 0.23, p=0.23)].Conclusion: The low ADAM8 plasma levels in children with ASD possibly indicated that ADAM8 might be implicated in the pathogenesis of ASD but not in the severity of the disease. These results should be interpreted with caution until additional studies are carried out with larger populations to decide whether the reduction in plasma ADAM8 levels is a mere consequence of ASD or if it plays a pathogenic role in the disease.Keywords: autism spectrum disorder, neuroinflammation, a disintegrin and metalloprotease 8, neurodevelopmental disorde

From the genetic architecture to synaptic plasticity in autism spectrum disorder.

International audienceGenetics studies of autism spectrum disorder (ASD) have identified several risk genes that are key regulators of synaptic plasticity. Indeed, many of the risk genes that have been linked to these disorders encode synaptic scaffolding proteins, receptors, cell adhesion molecules or proteins that are involved in chromatin remodelling, transcription, protein synthesis or degradation, or actin cytoskeleton dynamics. Changes in any of these proteins can increase or decrease synaptic strength or number and, ultimately, neuronal connectivity in the brain. In addition, when deleterious mutations occur, inefficient genetic buffering and impaired synaptic homeostasis may increase an individual's risk for ASD