Human Soluble Amyloid Precursor Protein β ELISA kit

We propose that giant flares on soft gamma-ray repeaters produce relativistic, strongly magnetized, weakly baryon-loaded magnetic clouds, somewhat analogous to solar coronal mass ejection (CME) events. The flares are driven by unwinding of the internal non-potential magnetic field which leads to a slow build-up of magnetic energy outside of the neutron star. For large magnetospheric currents, corresponding to a large twist of the external magnetic field, the magnetosphere becomes dynamically unstable on the Alfven crossing time-scale of the inner magnetosphere, t(A)similar to R-NS/c similar to 30 mu s. The dynamic instability leads to the formation of dissipative current sheets through the development of a tearing mode. The released magnetic energy results in the formation of a strongly magnetized, pair-loaded, quasi-spherically expanding flux rope, topologically connected by the magnetic field to the neutron star during the prompt flare emission. The expansion reaches large Lorentz factors, Gamma similar to 10-20, at distances r similar to 1-2 x 10(7) cm, where a leptophotonic load is lost. Beyond this radius plasma is strongly dominated by the magnetic field, though some baryon loading, with M < E/c(2), by ablated neutron star material may occur. Magnetic stresses of the tied flux rope lead to a late collimation of the expansion, on time-scales longer than the giant flare duration. Relativistic bulk motion of the expanding magnetic cloud, directed at an angle theta similar to 135 degrees to the line of sight (away from the observer), results in a strongly non-spherical forward shock with observed non-relativistic apparent expansion and bulk motion velocities beta(app)similar to cot theta/2 similar to 0.4 at times of the first radio observations, approximately one week after the burst. An interaction with a shell of wind-shocked interstellar medium (ISM) and then with the unshocked ISM leads to a deceleration, to non-relativistic velocities approximately one month after the flare.

Presenilin enhancer-2 (PSENEN) is a fundamental component of the T-secretase protein complex involved in beta-amyloid precursor protein (beta APP) processing, a key event in Alzheimer's disease (AD) etiopathogenesis. In a mild cognitive impairment (MCI)-diagnosed woman, belonging to a family with a positive history for AD, we found that a novel PSENEN mutation (S73F) was the only genetic alteration of relevance. The mutation was absent in 253 age-matched controls. In an attempt to learn the biochemical effects of this mutation, we Cultured skin primary fibroblasts from the patient and her daughter, and we assessed A beta(1-40) and A beta(1-42) production. We did not find any relevant differences in comparison to age-matched, normal subjects. Although our data do not definitively support a pathogenetic role for this mutation, it does not appear to be a common polymorphism. Further follow-up is warranted in this family. (C) 2007 The Alzheimer's Association. All rights reserved.