Kinetic and Products Study of the Atmospheric Degradation of trans-2-Hexenal with Cl Atoms

The gas-phase reaction between trans-2-hexenal (T2H) and chlorine atoms (Cl) was studied using three complementary experimental setups at atmospheric pressure and room temperature. In this work, we studied the rate constant for the titled oxidation reaction as well as the formation of the gas-phase products and secondary organic aerosols (SOAs). The rate constant of the T2H + Cl reaction was determined using the relative method in a simulation chamber using proton-transfer reaction time-of-flight mass spectrometry (PTR-ToF-MS) to monitor the loss of T2H and the reference compound. An average reaction rate constant of (3.17 ± 0.72) × 10–10 cm3 molecule–1 s–1 was obtained. From this, the atmospheric lifetime of T2H due to Cl reaction was estimated to be 9 h for coastal regions. HCl, CO, and butanal were identified as primary products using Fourier transform infrared spectroscopy (FTIR). The molar yield of butanal was (6.4 ± 0.3)%. Formic acid was identified as a secondary product by FTIR. In addition, butanal, 2-chlorohexenal, and 2-hexenoic acid were identified as products by gas chromatography coupled to mass spectrometry but not quantified. A reaction mechanism is proposed based on the observed products. SOA formation was observed by using a fast mobility particle sizer spectrometer. The measured SOA yields reached maximum values of about 38% at high particle mass concentrations. This work exhibits for the first time that T2H can be a source of SOA in coastal atmospheres, where Cl concentrations can be high at dawn, or in industrial areas, such as ceramic industries, where Cl precursors may be present.La reacción en fase gaseosa entre el trans-2-hexenal (T2H) y átomos de cloro (Cl) se estudió utilizando tres montajes experimentales complementarios a presión atmosférica y temperatura ambiente. En este trabajo se estudió la constante de velocidad de la reacción de oxidación titulada, así como la formación de los productos en fase gaseosa y los aerosoles orgánicos secundarios (SOAs). La constante de velocidad de la reacción T2H + Cl se determinó mediante el método relativo en una cámara de simulación utilizando espectrometría de masas de tiempo de vuelo de reacción de transferencia de protones (PTR-ToF-MS) para monitorizar la pérdida de T2H y del compuesto de referencia. Se obtuvo una constante de velocidad de reacción media de (3,17 ± 0,72) × 10-10 cm3 molécula-1 s-1 . A partir de ella, se estimó que la vida atmosférica de T2H debida a la reacción con Cl era de 9 h para las regiones costeras. Se identificaron HCl, CO y butanal como productos primarios mediante espectroscopia infrarroja por transformada de Fourier (FTIR). El rendimiento molar de butanal fue de (6,4 ± 0,3)%. El ácido fórmico se identificó como producto secundario mediante FTIR. Además, se identificaron butanal, 2-clorohexenal y ácido 2-hexenoico como productos mediante cromatografía de gases acoplada a espectrometría de masas, pero no se cuantificaron. Se propone un mecanismo de reacción basado en los productos observados. La formación de SOA se observó utilizando un espectrómetro de partículas de movilidad rápida. Los rendimientos de SOA medidos alcanzaron valores máximos de alrededor del 38% a altas concentraciones de masa de partículas. Este trabajo muestra por primera vez que el T2H puede ser una fuente de SOA en atmósferas costeras, donde las concentraciones de Cl pueden ser elevadas al amanecer, o en áreas industriales, como las industrias cerámicas, donde pueden estar presentes precursores de Cl

Reaction of OH radicals with CH3NH2 in the gas phase: experimental (11.7–177.5 K) and computed rate coefficients (10–1000 K)

Nitrogen-bearing molecules, like methylamine (CH3NH2), can be the building blocks of amino acids in the interstellar medium (ISM). At the ultralow temperatures of the ISM, it is important to know its gas-phase reactivity towards interstellar radicals and the products formed. In this work, the kinetics of the OH + CH3NH2 reaction was experimentally and theoretically investigated at low- and high-pressure limits (LPL and HPL) between 10 and 1000 K. Moreover, the CH2NH2 and CH3NH yields were computed in the same temperature range for both pressure regimes. A pulsed CRESU (French acronym for Reaction Kinetics in a Uniform Supersonic Flow) apparatus was employed to determine the rate coefficient, k(T), in the 11.7–177.5 K range. A drastic increase of k(T) when the temperature is lowered was observed in agreement with theoretical calculations, evaluated by the competitive canonical unified statistical (CCUS) theory, below 300 K in the LPL regime. The same trend was observed in the HPL regime below 350 K, but the theoretical k(T) values were higher than the experimental ones. Above 200 K, the calculated rate coefficients are improved with respect to previous computational studies and are in excellent agreement with the experimental literature data. In the LPL, the formation of CH3NH becomes largely dominant below ca. 100 K. Conversely, in the HPL regime, CH2NH2 is the only product below 100 K, whereas CH3NH becomes dominant at 298 K with a branching ratio similar to the one found in the LPL regime (≈70%). At T > 300 K, both reaction channels are competitive independently of the pressure regimeLas moléculas que contienen nitrógeno, como la metilamina (CH 3 NH 2 ), pueden ser los componentes básicos de los aminoácidos en el medio interestelar (ISM). A las temperaturas ultrabajas del ISM, es importante conocer su reactividad en fase gaseosa hacia los radicales interestelares y los productos formados. En este trabajo se investigó experimental y teóricamente la cinética de la reacción OH + CH 3 NH 2 a límites de baja y alta presión (LPL y HPL) entre 10 y 1000 K. Además, las reacciones CH 2 NH 2 y CH 3Los rendimientos de NH se calcularon en el mismo rango de temperatura para ambos regímenes de presión. Se empleó un aparato CRESU (acrónimo francés de Reaction Kinetics in a Uniform Supersonic Flow) pulsado para determinar el coeficiente de velocidad, k ( T ), en el rango de 11,7–177,5 K. De acuerdo con los cálculos teóricos, evaluados por la teoría de la estadística unificada canónica competitiva (CCUS), se observó un aumento drástico de k ( T ) cuando se baja la temperatura, por debajo de 300 K en el régimen LPL. La misma tendencia se observó en el régimen HPL por debajo de 350 K, pero el k teórico ( T) los valores fueron superiores a los experimentales. Por encima de 200 K, los coeficientes de velocidad calculados mejoran con respecto a estudios computacionales previos y están en excelente acuerdo con los datos de la literatura experimental. En el LPL, la formación de CH 3 NH se vuelve mayoritariamente dominante por debajo de ca. 100 K. Por el contrario, en el régimen HPL, CH 2 NH 2 es el único producto por debajo de 100 K, mientras que CH 3 NH se vuelve dominante a 298 K con una relación de ramificación similar a la encontrada en el régimen LPL (≈70%). A T > 300 K, ambos canales de reacción son competitivos independientemente del régimen de presión

Common and rare variant association analyses in amyotrophic lateral sclerosis identify 15 risk loci with distinct genetic architectures and neuron-specific biology

A cross-ancestry genome-wide association meta-analysis of amyotrophic lateral sclerosis (ALS) including 29,612 patients with ALS and 122,656 controls identifies 15 risk loci with distinct genetic architectures and neuron-specific biology. Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with a lifetime risk of one in 350 people and an unmet need for disease-modifying therapies. We conducted a cross-ancestry genome-wide association study (GWAS) including 29,612 patients with ALS and 122,656 controls, which identified 15 risk loci. When combined with 8,953 individuals with whole-genome sequencing (6,538 patients, 2,415 controls) and a large cortex-derived expression quantitative trait locus (eQTL) dataset (MetaBrain), analyses revealed locus-specific genetic architectures in which we prioritized genes either through rare variants, short tandem repeats or regulatory effects. ALS-associated risk loci were shared with multiple traits within the neurodegenerative spectrum but with distinct enrichment patterns across brain regions and cell types. Of the environmental and lifestyle risk factors obtained from the literature, Mendelian randomization analyses indicated a causal role for high cholesterol levels. The combination of all ALS-associated signals reveals a role for perturbations in vesicle-mediated transport and autophagy and provides evidence for cell-autonomous disease initiation in glutamatergic neurons

Common and rare variant association analyses in amyotrophic lateral sclerosis identify 15 risk loci with distinct genetic architectures and neuron-specific biology

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with a lifetime risk of one in 350 people and an unmet need for disease-modifying therapies. We conducted a cross-ancestry genome-wide association study (GWAS) including 29,612 patients with ALS and 122,656 controls, which identified 15 risk loci. When combined with 8,953 individuals with whole-genome sequencing (6,538 patients, 2,415 controls) and a large cortex-derived expression quantitative trait locus (eQTL) dataset (MetaBrain), analyses revealed locus-specific genetic architectures in which we prioritized genes either through rare variants, short tandem repeats or regulatory effects. ALS-associated risk loci were shared with multiple traits within the neurodegenerative spectrum but with distinct enrichment patterns across brain regions and cell types. Of the environmental and lifestyle risk factors obtained from the literature, Mendelian randomization analyses indicated a causal role for high cholesterol levels. The combination of all ALS-associated signals reveals a role for perturbations in vesicle-mediated transport and autophagy and provides evidence for cell-autonomous disease initiation in glutamatergic neurons. A cross-ancestry genome-wide association meta-analysis of amyotrophic lateral sclerosis (ALS) including 29,612 patients with ALS and 122,656 controls identifies 15 risk loci with distinct genetic architectures and neuron-specific biology

Analysis of shared common genetic risk between amyotrophic lateral sclerosis and epilepsy

Because hyper-excitability has been shown to be a shared pathophysiological mechanism, we used the latest and largest genome-wide studies in amyotrophic lateral sclerosis (n = 36,052) and epilepsy (n = 38,349) to determine genetic overlap between these conditions. First, we showed no significant genetic correlation, also when binned on minor allele frequency. Second, we confirmed the absence of polygenic overlap using genomic risk score analysis. Finally, we did not identify pleiotropic variants in meta-analyses of the 2 diseases. Our findings indicate that amyotrophic lateral sclerosis and epilepsy do not share common genetic risk, showing that hyper-excitability in both disorders has distinct origins

Common and rare variant association analyses in amyotrophic lateral sclerosis identify 15 risk loci with distinct genetic architectures and neuron-specific biology

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with a lifetime risk of one in 350 people and an unmet need for disease-modifying therapies. We conducted a cross-ancestry genome-wide association study (GWAS) including 29,612 patients with ALS and 122,656 controls, which identified 15 risk loci. When combined with 8,953 individuals with whole-genome sequencing (6,538 patients, 2,415 controls) and a large cortex-derived expression quantitative trait locus (eQTL) dataset (MetaBrain), analyses revealed locus-specific genetic architectures in which we prioritized genes either through rare variants, short tandem repeats or regulatory effects. ALS-associated risk loci were shared with multiple traits within the neurodegenerative spectrum but with distinct enrichment patterns across brain regions and cell types. Of the environmental and lifestyle risk factors obtained from the literature, Mendelian randomization analyses indicated a causal role for high cholesterol levels. The combination of all ALS-associated signals reveals a role for perturbations in vesicle-mediated transport and autophagy and provides evidence for cell-autonomous disease initiation in glutamatergic neurons. A cross-ancestry genome-wide association meta-analysis of amyotrophic lateral sclerosis (ALS) including 29,612 patients with ALS and 122,656 controls identifies 15 risk loci with distinct genetic architectures and neuron-specific biology

Common and rare variant association analyses in amyotrophic lateral sclerosis identify 15 risk loci with distinct genetic architectures and neuron-specific biology

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with a lifetime risk of one in 350 people and an unmet need for disease-modifying therapies. We conducted a cross-ancestry genome-wide association study (GWAS) including 29,612 patients with ALS and 122,656 controls, which identified 15 risk loci. When combined with 8,953 individuals with whole-genome sequencing (6,538 patients, 2,415 controls) and a large cortex-derived expression quantitative trait locus (eQTL) dataset (MetaBrain), analyses revealed locus-specific genetic architectures in which we prioritized genes either through rare variants, short tandem repeats or regulatory effects. ALS-associated risk loci were shared with multiple traits within the neurodegenerative spectrum but with distinct enrichment patterns across brain regions and cell types. Of the environmental and lifestyle risk factors obtained from the literature, Mendelian randomization analyses indicated a causal role for high cholesterol levels. The combination of all ALS-associated signals reveals a role for perturbations in vesicle-mediated transport and autophagy and provides evidence for cell-autonomous disease initiation in glutamatergic neurons.peer-reviewe

Etude experimentale des rapports de branchement issus de la recombinaison dissociative d'ions polyatomiques avec des electrons. Mesure de la vitesse de recombinaison dissociative des ions O_2"+, N_2"+ et H_3"+ a 300 K

SIGLEAvailable from INIST (FR), Document Supply Service, under shelf-number : T 78731 / INIST-CNRS - Institut de l'Information Scientifique et TechniqueFRFranc

The radiative association of CH with H₂: a mechanism for formation of CH₃ in interstellar clouds

International audienc

Analysis of shared common genetic risk between amyotrophic lateral sclerosis and epilepsy

Because hyper-excitability has been shown to be a shared pathophysiological mechanism, we used the latest and largest genome-wide studies in amyotrophic lateral sclerosis (n = 36,052) and epilepsy (n = 38,349) to determine genetic overlap between these conditions. First, we showed no significant genetic correlation, also when binned on minor allele frequency. Second, we confirmed the absence of polygenic overlap using genomic risk score analysis. Finally, we did not identify pleiotropic variants in meta-analyses of the 2 diseases. Our findings indicate that amyotrophic lateral sclerosis and epilepsy do not share common genetic risk, showing that hyper-excitability in both disorders has distinct origins