12 research outputs found
Study of a Bisquaternary Ammonium Salt by Atmospheric Pressure Photoionization Mass Spectrometry
The Formation of Protonated Dimethyl Ether from the Metastable Molecular Ions of 1-Methoxy-2-Propanol, CH 3
The gas-phase basicity and proton affinity of 1,3,5-cycloheptatriene - energetics, structure and interconversion of dihydrotropylium ions
Salpin J-Y, Mormann M, Tortajada J, Nguyen M-T, Kuck D. The gas-phase basicity and proton affinity of 1,3,5-cycloheptatriene - energetics, structure and interconversion of dihydrotropylium ions. EUROPEAN JOURNAL OF MASS SPECTROMETRY. 2003;9(1):361-376.The hitherto unknown gas-phase basicity and proton affinity of 1,3,5-cycloheptatriene (CHT) have been determined by Fourier transform ion cyclotron resonance (FT-ICR) mass spectrometry. Several independent techniques were used in order to exclude ambiguities due to proton-induced isomerisation of the conjugate cyclic C7H9+ ions, [CHT + H](+). The gas-phase basicity obtained by the thermokinetic method, GB(CHT) = 799 +/- 4 kJ mol(-1), was found to be identical, within the limits of experimental error, with the values measured by the equilibrium method starting with protonated reference bases, and with the values resulting from the measurements of the individual forward and reverse rate constants, when corrections were made for the isomerised fraction of the C7H9+ population. The experimentally determined gas-phase basicity leads to the proton affinity of cycloheptatriene, PA(CHT) = 833 +/- 4 kJ mol(-1), and the heat of formation of the cyclo-C7H9+ ion, DeltaH(r)(0)([CHT + H](+)) = 884 +/- 4 kJ mol(-1). Ab initio calculations are in agreement with these experimental values if the 1,2-dihydrotropylium tautomer, [CHT + H-(1)](+), generated by protonation of CHT at C-1, is assumed to be the conjugate acid, resulting in PA(CHT) = 825 +/- 2 kJ mol(-1) and DeltaH(f 300)degrees([CHT + H-(1)](+)) = 892 +/- 2 kJ mol(-1). However, the calculations indicate that protonation of cycloheptatriene at C-2 gives rise to transannular C-C bond formation, generating protonated norcaradiene [NCD + H](+), a valence tautomer being 19 kJ mol(-1) more stable than [CHT + H-(1)](+). The 1,4-dihydrotropylium ion, [CHT + H-(3)](+), generated by protonation of CHT at C-3, is 17 kJ mol(-1) less stable than [CHT + H-(2)](+). The bicyclic isomer [NCD + H](+) is separated by relatively high barriers, 70 and 66 kJ mol(-1) from the monocyclic isomers, [CHT + H-(1)](+) and [CHT + H-(3)](+), respectively. Therefore, the initially formed 1,2-dihydrotropylium ion [CHT + H-(1)](+) does not rearrange to the bicyclic isomer [NCD + H](+) under mild protonation conditions
A Review of the Hyporheic Zone, Stream Restoration, and Means to Enhance Denitrification
Benzene Oxidation: Experimental Results in a JDR and Comprehensive Kinetic Modeling in JSR, Shock-Tube and Flame
Clinical associations and time of onset of cerebral white matter damage in very preterm babies.
Birbeck Granules Are Subdomains of Endosomal Recycling Compartment in Human Epidermal Langerhans Cells, Which Form Where Langerin Accumulates
Birbeck granules are unusual rod-shaped structures specific to epidermal Langerhans cells, whose origin and function remain undetermined. We investigated the intracellular location and fate of Langerin, a protein implicated in Birbeck granule biogenesis, in human epidermal Langerhans cells. In the steady state, Langerin is predominantly found in the endosomal recycling compartment and in Birbeck granules. Langerin internalizes by classical receptor-mediated endocytosis and the first Birbeck granules accessible to endocytosed Langerin are those connected to recycling endosomes in the pericentriolar area, where Langerin accumulates. Drug-induced inhibition of endocytosis results in the appearance of abundant open-ended Birbeck granule-like structures appended to the plasma membrane, whereas inhibition of recycling induces Birbeck granules to merge with a tubular endosomal network. In mature Langerhans cells, Langerin traffic is abolished and the loss of internal Langerin is associated with a concomitant depletion of Birbeck granules. Our results demonstrate an exchange of Langerin between early endosomal compartments and the plasma membrane, with dynamic retention in the endosomal recycling compartment. They show that Birbeck granules are not endocytotic structures, rather they are subdomains of the endosomal recycling compartment that form where Langerin accumulates. Finally, our results implicate ADP-ribosylation factor proteins in Langerin trafficking and the exchange between Birbeck granules and other endosomal membranes
Uncovering the genetic architecture of broad antisocial behavior through a genome-wide association study meta-analysis.
Despite the substantial heritability of antisocial behavior (ASB), specific genetic variants robustly associated with the trait have not been identified. The present study by the Broad Antisocial Behavior Consortium (BroadABC) meta-analyzed data from 28 discovery samples (N = 85,359) and five independent replication samples (N = 8058) with genotypic data and broad measures of ASB. We identified the first significant genetic associations with broad ASB, involving common intronic variants in the forkhead box protein P2 (FOXP2) gene (lead SNP rs12536335, p = 6.32 × 10 <sup>-10</sup> ). Furthermore, we observed intronic variation in Foxp2 and one of its targets (Cntnap2) distinguishing a mouse model of pathological aggression (BALB/cJ strain) from controls (BALB/cByJ strain). Polygenic risk score (PRS) analyses in independent samples revealed that the genetic risk for ASB was associated with several antisocial outcomes across the lifespan, including diagnosis of conduct disorder, official criminal convictions, and trajectories of antisocial development. We found substantial genetic correlations of ASB with mental health (depression r <sub>g</sub> = 0.63, insomnia r <sub>g</sub> = 0.47), physical health (overweight r <sub>g</sub> = 0.19, waist-to-hip ratio r <sub>g</sub> = 0.32), smoking (r <sub>g</sub> = 0.54), cognitive ability (intelligence r <sub>g</sub> = -0.40), educational attainment (years of schooling r <sub>g</sub> = -0.46) and reproductive traits (age at first birth r <sub>g</sub> = -0.58, father's age at death r <sub>g</sub> = -0.54). Our findings provide a starting point toward identifying critical biosocial risk mechanisms for the development of ASB