Study of excited states in49V with the48Ti (p, γ)49V reaction

In the⁴⁸Ti(p, γ)⁴⁹V reaction gamma decays of thirteen resonances betweenE _p =960 and 1570 keV are investigated. Level energies within ±0.5–±2.0 keV andQ-value 6756.8±1.5 keV are obtained. Branching ratios for the resonance states and strongly populated bound states are given. Gamma-ray angular distribution measurements yield the followingJ(keV) assignments of⁴⁹V bound and resonance states:J(1140)=5/2,J ^π(2235)=5/2^(?),J(2264)=(3/2),J(2308)=3/2,J(3912)=3/2,J(8105,Ep=1374keV)=(1/2) andJ ^π(8289,E _p =1564keV)=3/2^(?). Multipolarity mixing ratios for all measured primary and secondary gamma rays are tabulated. Dopplershift attenuation measurements yield the mean lifetimes τ _m (keV) of the following bound states in⁴⁹V:τ _m (748)=(200± ₁₀₀ ⁴⁰⁰ )fs, τ _m (1140)=(250± ₁₀₀ ⁵⁰⁰ )fs, τ _m (1155)>400 fs, τ _m (1515)=(45± ₂₀ ³⁰ )fs, τ _m (1644)=(55± ₂₀ ³⁰ )fs, τ _m (1661)=(25±5)fs, τ _m (1994)>400 fs, τ _m (2235)=(30± ₁₅ ³⁰ )fs, τ _m (2264)=(45± ₁₅ ³⁰ )fs and τ _m (2308)=(20±10)fs.     

Dichlorocarbene Addition to

In contrast to the terminal phosphinidene complex PhPW(CO)(5) (2), which adds to [5]metacyclophane (1) in a 1,4-fashion, dichlorocarbene preferentially adds in a 1,2-fashion to the formal "anti-Bredt" type double bond of the aromatic ring of 1 to afford the norcaradiene 11b, which immediately rearranges to the bridged cycloheptatriene 12b and further by a [1,5] sigmatropic chlorine migration to the isomeric 13b as the first observable product. More slowly, the latter isomerizes via a dissociative mechanism to give 15b. A computational study supports the notion that the [1,5] chlorine migration in the rearrangement 12b --> 13b, for which an activation barrier of 70.2 kJ mol(-)(1) was calculated, is essentially concerted with minor charge separation. In contrast, the analogous [1,5] chlorine migration in the flat model compound 7,7-dichlorocycloheptatriene (12a) displays features of a dissociative pathway.     

FiD: a software for ab initio structural identification of product ions from tandem mass spectrometric data

We present FiD (Fragment iDentificator), a software tool for the structural identification of product ions produced with tandem mass spectrometric measurement of low molecular weight organic compounds. Tandem mass spectrometry (MS/MS) has proven to be an indispensable tool in modern, cell-wide metabolomics and fluxomics studies. In such studies, the structural information of the MS(n) product ions is usually needed in the downstream analysis of the measurement data. The manual identification of the structures of MS(n) product ions is, however, a nontrivial task requiring expertise, and calls for computer assistance. Commercial software tools, such as Mass Frontier and ACD/MS Fragmenter, rely on fragmentation rule databases for the identification of MS(n) product ions. FiD, on the other hand, conducts a combinatorial search over all possible fragmentation paths and outputs a ranked list of alternative structures. This gives the user an advantage in situations where the MS/MS data of compounds with less well-known fragmentation mechanisms are processed. FiD software implements two fragmentation models, the single-step model that ignores intermediate fragmentation states and the multi-step model, which allows for complex fragmentation pathways. The software works for MS/MS data produced both in positive- and negative-ion modes. The software has an easy-to-use graphical interface with built-in visualization capabilities for structures of product ions and fragmentation pathways. In our experiments involving amino acids and sugar-phosphates, often found, e.g., in the central carbon metabolism of yeasts, FiD software correctly predicted the structures of product ions on average in 85% of the cases. The FiD software is free for academic use and is available for download from www.cs.helsinki.fi/group/sysfys/software/fragid. Copyright (c) 2008 John Wiley & Sons, Ltd.     

ALS-associated mutant SOD1<Superscript>G93A</Superscript> causes mitochondrial vacuolation by expansion of the intermembrane space and by involvement of SOD1 aggregation and peroxisomes

Background  

Amyotrophic lateral sclerosis (ALS) is an age-dependent neurodegenerative disease that causes motor neuron degeneration, paralysis and death. Mutations in Cu, Zn superoxide dismutase (SOD1) are one cause for the familial form of this disease. Transgenic mice expressing mutant SOD1 develop age-dependent motor neuron degeneration, skeletal muscle weakness, paralysis and death similar to humans. The mechanism whereby mutant SOD1 induces motor neuron degeneration is not understood but widespread mitochondrial vacuolation has been observed during early phases of motor neuron degeneration. How this vacuolation develops is not clear, but could involve autophagic vacuolation, mitochondrial permeability transition (MPT) or uncharacterized mechanisms. To determine which of these possibilities are true, we examined the vacuolar patterns in detail in transgenic mice expressing mutant SOD1^G93A.