Recoil correction to the bound-electron g factor in H-like atoms to all orders in αZ\alpha Z

The nuclear recoil correction to the bound-electron g factor in H-like atoms is calculated to first order in $m/M$ and to all orders in $\alpha Z$. The calculation is performed in the range Z=1-100. A large contribution of terms of order $(\alpha Z)^5$ and higher is found. Even for hydrogen, the higher-order correction exceeds the $(\alpha Z)^4$ term, while for uranium it is above the leading $(\alpha Z)^2$ correction.Comment: 6 pages, 3 tables, 1 figur

Recoil correction to the ground state energy of hydrogenlike atoms

The recoil correction to the ground state energy of hydrogenlike atoms is calculated to all orders in \alpha Z in the range Z = 1-110. The nuclear size corrections to the recoil effect are partially taken into account. In the case of hydrogen, the relativistic recoil correction beyond the Salpeter contribution and the nonrelativistic nuclear size correction to the recoil effect, amounts to -7.2(2) kHz. The total recoil correction to the ground state energy in hydrogenlike uranium (^{238}U^{91+}) constitutes 0.46 eV.Comment: 16 pages, 1 figure (eps), Latex, submitted to Phys.Rev.

Complete two-loop correction to the bound-electron g factor

Within a systematic approach based on the dimensionally regularized nonrelativistic quantum electrodynamics, we derive the complete result for the two-loop correction to order $(\alpha/\pi)^2 (Z \alpha)^4$ for the $g$ factor of an electron bound in an $nS$ state of a hydrogenlike ion. The results obtained significantly improve the accuracy of the theoretical predictions for the hydrogenlike carbon and oxygen ions and influence the value of the electron mass inferred from $g$ factor measurements.Comment: 11 pages, 1 figur

Screened self-energy correction to the 2p3/2-2s transition energy in Li-like ions

We present an ab initio calculation of the screened self-energy correction for (1s)^2 2p3/2 and (1s)^2 2s states of Li-like ions with nuclear charge numbers in the range Z = 12-100. The evaluation is carried out to all orders in the nuclear-strength parameter Z \alpha. This investigation concludes our calculations of all two-electron QED corrections for the 2p3/2-2s transition energy in Li-like ions and thus considerably improves theoretical predictions for this transition for high-Z ions

The Atg1-kinase complex tethers Atg9-vesicles to initiate autophagy

Autophagosomes are double-membrane vesicles that sequester cytoplasmic material for lysosomal degradation. Their biogenesis is initiated by recruitment of Atg9-vesicles to the phagophore assembly site. This process depends on the regulated activation of the Atg1-kinase complex. However, the underlying molecular mechanism remains unclear. Here we reconstitute this early step in autophagy from purified components in vitro. We find that on assembly from its cytoplasmic subcomplexes, the Atg1-kinase complex becomes activated, enabling it to recruit and tether Atg9-vesicles. The scaffolding protein Atg17 targets the Atg1-kinase complex to autophagic membranes by specifically recognizing the membrane protein Atg9. This interaction is inhibited by the two regulatory subunits Atg31 and Atg29. Engagement of the Atg1-Atg13 subcomplex restores the Atg9-binding and membrane-tethering activity of Atg17. Our data help to unravel the mechanism that controls Atg17-mediated tethering of Atg9-vesicles, providing the molecular basis to understand initiation of autophagosome-biogenesis

Evidence for the absence of regularization corrections to the partial-wave renormalization procedure in one-loop self energy calculations in external fields

The equivalence of the covariant renormalization and the partial-wave renormaliz ation (PWR) approach is proven explicitly for the one-loop self-energy correction (SE) of a bound electron state in the presence of external perturbation potentials. No spurious correctio n terms to the noncovariant PWR scheme are generated for Coulomb-type screening potentia ls and for external magnetic fields. It is shown that in numerical calculations of the SE with Coulombic perturbation potential spurious terms result from an improper treatment of the unphysical high-energy contribution. A method for performing the PWR utilizing the relativistic B-spline approach for the construction of the Dirac spectrum in external magnetic fields is proposed. This method is applied for calculating QED corrections to the bound-electron $g$-factor in H-like ions. Within the level of accuracy of about 0.1% no spurious terms are generated in numerical calculations of the SE in magnetic fields.Comment: 22 pages, LaTeX, 1 figur

Chemical Evolution of Calc-alkaline Magmas during the Ascent through Continental Crust: Constraints from Methana, Aegean Arc

M1 - egaa036Quaternary calc-alkaline andesitic to dacitic lavas effusively erupted on top of about 30 km thick accreted continental crust at Methana peninsula in the western Aegean arc. We present new data of major and trace element concentrations as well as of Sr-Nd-Pb isotope ratios along with mineral compositions of Methana lavas and their mafic enclaves. The enclaves imply a parental basaltic magma and fractional crystallization processes with relatively little crustal assimilation in the deep part of the Methana magma system. The composition of amphibole in some mafic enclaves and lavas indicates deeper crystallization at similar to 25km depth close to the Moho compared with the evolved lavas that formed atPeer reviewe

TECPR1 promotes aggrephagy by direct recruitment of LC3C autophagosomes to lysosomes

The accumulation of protein aggregates is involved in the onset of many neurodegenerative diseases. Aggrephagy is a selective type of autophagy that counteracts neurodegeneration by degrading such aggregates. In this study, we found that LC3C cooperates with lysosomal TECPR1 to promote the degradation of disease-related protein aggregates in neural stem cells. The N-terminal WD-repeat domain of TECPR1 selectively binds LC3C which decorates matured autophagosomes. The interaction of LC3C and TECPR1 promotes the recruitment of autophagosomes to lysosomes for degradation. Augmented expression of TECPR1 in neural stem cells reduces the number of protein aggregates by promoting their autophagic clearance, whereas knockdown of LC3C inhibits aggrephagy. The PH domain of TECPR1 selectively interacts with PtdIns(4)P to target TECPR1 to PtdIns(4)P containing lysosomes. Exchanging the PH against a tandem-FYVE domain targets TECPR1 ectopically to endosomes. This leads to an accumulation of LC3C autophagosomes at endosomes and prevents their delivery to lysosomes. Many neurodegenerative disorders are characterised by the accumulation of protein aggregates in neurons. Here, the authors show that the lysosomal protein TECPR1 selectively recruits mature autophagosomes via an interaction with LC3C to break down protein aggregates in neural stem cells