Statistics of Neutron Stars at the Stage of Supersonic Propeller

We analyze the statistical distribution of neutron stars at the stage of a supersonic propeller. An important point of our analysis is allowance for the evolution of the angle of inclination of the magnetic axis to the spin axis of the neutron star for the boundary of the transition to the supersonic propeller stage for two models: the model with hindered particle escape from the stellar surface and the model with free particle escape. As a result, we have shown that a consistent allowance for the evolution of the inclination angle in the region of extinct radio pulsars for the two models leads to an increase in the total number of neutron stars at the supersonic propeller stage. This increase stems from he fact that when allowing for the evolution of the inclination angle $\chi$ for neutron stars in the region of extinct radio pulsars and, hence, for the boundary of the transition to the propeller stage, this transition is possible at shorter spin periods (P~5-10 s) than assumed in the standard model.Comment: 15 pages, 6 figures; scale corrected for figures 3-

ВЛИЯНИЕ ПОЛИМОРФНЫХ ВАРИАНТОВ ГЕНА АПОЛИПОПРОТЕИНА А-I НА ЛИПИДНЫЙ СПЕКТР ПЛАЗМЫ КРОВИ В ПОПУЛЯЦИИ САНКТ-ПЕТЕРБУРГА

Apolipoprotein A-I is a key structure protein of antiatherogenic high density lipoproteins (HDL). The aim of the study was to investigate the relationship between (-75)G/A and 83C/T polymorphic variants of apolipoprotein A-I gene (APOA1) and the plasma lipid profile in the population of Saint-Petersburg. Allele T83 of APOA1 gene was found to be associated with the reduced risk of atherosclerosis development among Saint-Petersburg inhabitants. The study demonstrates that allele T83 of APOA1 gene is associated with higher plasma HDL cholesterol levels (pАполипопротеин А-I является основным структурным белком антиатерогенных липопротеинов высокой плотности (ЛПВП). Целью исследования явился анализ корреляции полиморфных вариантов (-75) G/A и 83C/T гена APOA1 с уровнем липидов плазмы крови в популяции Санкт-Петербурга. Было установлено, что аллель T83 гена APOA1, ассоциированный со снижением риска развития атеросклероза у жителей Санкт-Петербурга, характеризуется более высоким уровнем холестерина в составе ЛПВП (

Cosmology and Neutrino Properties

This is a brief review for particle physicists on cosmological impact of neutrinos and on restrictions on neutrino properties from cosmology. The paper includes discussion of upper bounds on neutrino mass and possible ways to relax them, methods to observe the cosmic neutrino background, bounds on the cosmological lepton asymmetry which are strongly improved by neutrino oscillations, cosmological effects of breaking of spin-statistics theorem for neutrinos, bounds on mixing parameters of active and possible sterile neutrinos with the account of active neutrino oscillations, bounds on right-handed currents and neutrino magnetic moments, and some more.Comment: Talk presented at the meeting of Nuclear Physics Division of Russian Academy of Sci., November, 2007, Moscow. 21 pages, 3 figures. One reference is added and some numbers are slightly correcte

Amyloid Oligomer Conformation in a Group of Natively Folded Proteins

Recent in vitro and in vivo studies suggest that destabilized proteins with defective folding induce aggregation and toxicity in protein-misfolding diseases. One such unstable protein state is called amyloid oligomer, a precursor of fully aggregated forms of amyloid. Detection of various amyloid oligomers with A11, an anti-amyloid oligomer conformation-specific antibody, revealed that the amyloid oligomer represents a generic conformation and suggested that toxic β-aggregation processes possess a common mechanism. By using A11 antibody as a probe in combination with mass spectrometric analysis, we identified GroEL in bacterial lysates as a protein that may potentially have an amyloid oligomer conformation. Surprisingly, A11 reacted not only with purified GroEL but also with several purified heat shock proteins, including human Hsp27, 40, 70, 90; yeast Hsp104; and bovine Hsc70. The native folds of A11-reactive proteins in purified samples were characterized by their anti-β-aggregation activity in terms of both functionality and in contrast to the β-aggregation promoting activity of misfolded pathogenic amyloid oligomers. The conformation-dependent binding of A11 with natively folded Hsp27 was supported by the concurrent loss of A11 reactivity and anti-β-aggregation activity of heat-treated Hsp27 samples. Moreover, we observed consistent anti-β-aggregation activity not only by chaperones containing an amyloid oligomer conformation but also by several A11-immunoreactive non-chaperone proteins. From these results, we suggest that the amyloid oligomer conformation is present in a group of natively folded proteins. The inhibitory effects of A11 antibody on both GroEL/ES-assisted luciferase refolding and Hsp70-mediated decelerated nucleation of Aβ aggregation suggested that the A11-binding sites on these chaperones might be functionally important. Finally, we employed a computational approach to uncover possible A11-binding sites on these targets. Since the β-sheet edge was a common structural motif having the most similar physicochemical properties in the A11-reactive proteins we analyzed, we propose that the β-sheet edge in some natively folded amyloid oligomers is designed positively to prevent β aggregation

Alzheimer disease models and human neuropathology: similarities and differences

Animal models aim to replicate the symptoms, the lesions or the cause(s) of Alzheimer disease. Numerous mouse transgenic lines have now succeeded in partially reproducing its lesions: the extracellular deposits of Aβ peptide and the intracellular accumulation of tau protein. Mutated human APP transgenes result in the deposition of Aβ peptide, similar but not identical to the Aβ peptide of human senile plaque. Amyloid angiopathy is common. Besides the deposition of Aβ, axon dystrophy and alteration of dendrites have been observed. All of the mutations cause an increase in Aβ 42 levels, except for the Arctic mutation, which alters the Aβ sequence itself. Overexpressing wild-type APP alone (as in the murine models of human trisomy 21) causes no Aβ deposition in most mouse lines. Doubly (APP × mutated PS1) transgenic mice develop the lesions earlier. Transgenic mice in which BACE1 has been knocked out or overexpressed have been produced, as well as lines with altered expression of neprilysin, the main degrading enzyme of Aβ. The APP transgenic mice have raised new questions concerning the mechanisms of neuronal loss, the accumulation of Aβ in the cell body of the neurons, inflammation and gliosis, and the dendritic alterations. They have allowed some insight to be gained into the kinetics of the changes. The connection between the symptoms, the lesions and the increase in Aβ oligomers has been found to be difficult to unravel. Neurofibrillary tangles are only found in mouse lines that overexpress mutated tau or human tau on a murine tau −/− background. A triply transgenic model (mutated APP, PS1 and tau) recapitulates the alterations seen in AD but its physiological relevance may be discussed. A number of modulators of Aβ or of tau accumulation have been tested. A transgenic model may be analyzed at three levels at least (symptoms, lesions, cause of the disease), and a reading key is proposed to summarize this analysis

Two-dimensional imaging of III-V quantum dots confinement potential

Composition, doping, size, and strain distribution within quantum dots, and at the dots-substrate interfaces, determine the confinement potential of electrons and holes creating a complex band structure. We use ultra-high vacuum Kelvin probe force microscopy to obtain the two-dimensional confinement potential in and around InAs and InSb dots epitaxially grown on GaAs. It is found that the potential manifests rich features governed by the strain and composition variations in the vicinity of the individual quantum dots. The results can adjust or confirm theoretical predictions for many epitaxial dots systems