Thermodynamics and reaction mechanism of urea decomposition

Selective catalytic reduction (SCR) for automotive applications depends on ammonia production from a urea-water solution by thermolysis and hydrolysis. In this process, undesired liquid and solid by-products are formed in the exhaust pipe. The formation and decomposition of these by-products have been studied by thermogravimetric analysis (TGA) and differential scanning calorimetry (DSC). Based on a previously published reaction mechanism by Brack et al. [1], a new reaction scheme is proposed that emphasizes the role of thermodynamic equilibrium of the reactants in liquid and solid phases [2]. The observed phenomenon of liquefaction and re-solidification of biuret in the temperature range 193–230 °C can be explained by formation of a eutectic mixture with urea. According to DSC data, the direct decomposition of urea to ammonia and isocyanic acid can be ruled out. The dominant route is a self-polymerisation of urea to biuret and triuret. Biuret and triuret decomposition are dominated by thermodynamic equilibria with gaseous isocyanic acid. For this, thermodynamic data of triuret have been refined. The apparent melting point of biuret at 193 °C is explained by the formation of a eutectic mixture within the urea-biuret-triuret-cyanuric acid ensemble. Furthermore, DSC data shows that cyanuric acid sublimates without decomposition at temperatures above 300 °C. Numerical simulations of the TGA and DSC experiments are performed by a multi-phase tank reactor model (DETCHEMMPTR [3]). The new reaction mechanism describes well the main features (decomposition steps and calorimetry) and dependencies (on heating rate and surface area) of the decompositions of urea, biuret, triuret and cyanuric acid. [1] W. Brack, B. Heine, F. Birkhold, M. Kruse, G. Schoch, S. Tischer and O. Deutschmann, “Kinetic modeling of urea decomposition based on systematic thermogravimetric analyses of urea and its most important by-products”, CES 106, 1–8 (2014). [2] S. Tischer, M. Börnhorst, J. Amsler, G. Schoch and O. Deutschmann, “Thermodynamics and reaction mechanism of urea decomposition”, PCCP, in press, DOI: 10.1039/C9CP01529A (2019). [3] www.detchem.co

Epilepsy, hippocampal sclerosis and febrile seizures linked by common genetic variation around SCN1A

Epilepsy comprises several syndromes, amongst the most common being mesial temporal lobe epilepsy with hippocampal sclerosis. Seizures in mesial temporal lobe epilepsy with hippocampal sclerosis are typically drug-resistant, and mesial temporal lobe epilepsy with hippocampal sclerosis is frequently associated with important co-morbidities, mandating the search for better understanding and treatment. The cause of mesial temporal lobe epilepsy with hippocampal sclerosis is unknown, but there is an association with childhood febrile seizures. Several rarer epilepsies featuring febrile seizures are caused by mutations in SCN1A, which encodes a brain-expressed sodium channel subunit targeted by many anti-epileptic drugs. We undertook a genome-wide association study in 1018 people with mesial temporal lobe epilepsy with hippocampal sclerosis and 7552 control subjects, with validation in an independent sample set comprising 959 people with mesial temporal lobe epilepsy with hippocampal sclerosis and 3591 control subjects. To dissect out variants related to a history of febrile seizures, we tested cases with mesial temporal lobe epilepsy with hippocampal sclerosis with (overall n = 757) and without (overall n = 803) a history of febrile seizures. Meta-analysis revealed a genome-wide significant association for mesial temporal lobe epilepsy with hippocampal sclerosis with febrile seizures at the sodium channel gene cluster on chromosome 2q24.3 [rs7587026, within an intron of the SCN1A gene, P = 3.36 × 10−9, odds ratio (A) = 1.42, 95% confidence interval: 1.26-1.59]. In a cohort of 172 individuals with febrile seizures, who did not develop epilepsy during prospective follow-up to age 13 years, and 6456 controls, no association was found for rs7587026 and febrile seizures. These findings suggest SCN1A involvement in a common epilepsy syndrome, give new direction to biological understanding of mesial temporal lobe epilepsy with hippocampal sclerosis with febrile seizures, and open avenues for investigation of prognostic factors and possible prevention of epilepsy in some children with febrile seizure

Epilepsy, hippocampal sclerosis and febrile seizures linked by common genetic variation around SCN1A.

Epilepsy comprises several syndromes, amongst the most common being mesial temporal lobe epilepsy with hippocampal sclerosis. Seizures in mesial temporal lobe epilepsy with hippocampal sclerosis are typically drug-resistant, and mesial temporal lobe epilepsy with hippocampal sclerosis is frequently associated with important co-morbidities, mandating the search for better understanding and treatment. The cause of mesial temporal lobe epilepsy with hippocampal sclerosis is unknown, but there is an association with childhood febrile seizures. Several rarer epilepsies featuring febrile seizures are caused by mutations in SCN1A, which encodes a brain-expressed sodium channel subunit targeted by many anti-epileptic drugs. We undertook a genome-wide association study in 1018 people with mesial temporal lobe epilepsy with hippocampal sclerosis and 7552 control subjects, with validation in an independent sample set comprising 959 people with mesial temporal lobe epilepsy with hippocampal sclerosis and 3591 control subjects. To dissect out variants related to a history of febrile seizures, we tested cases with mesial temporal lobe epilepsy with hippocampal sclerosis with (overall n = 757) and without (overall n = 803) a history of febrile seizures. Meta-analysis revealed a genome-wide significant association for mesial temporal lobe epilepsy with hippocampal sclerosis with febrile seizures at the sodium channel gene cluster on chromosome 2q24.3 [rs7587026, within an intron of the SCN1A gene, P = 3.36 × 10 -9, odds ratio (A) = 1.42, 95% confidence interval: 1.26-1.59]. In a cohort of 172 individuals with febrile seizures, who did not develop epilepsy during prospective follow-up to age 13 years, and 6456 controls, no association was found for rs7587026 and febrile seizures. These findings suggest SCN1A involvement in a common epilepsy syndrome, give new direction to biological understanding of mesial temporal lobe epilepsy with hippocampal sclerosis with febrile seizures, and open avenues for investigation of prognostic factors and possible prevention of epilepsy in some children with febrile seizures. © 2013 The Author (2013). Published by Oxford University Press on behalf of the Guarantors of Brain.0SCOPUS: ar.jinfo:eu-repo/semantics/publishe