1/f1/f noise in variable range hopping conduction

A mechanism of $1/f$ noise due to traps formed by impurities which have no neighbors with close energies in their vicinity is studied. Such traps slowly exchange electrons with the rest of conducting media. The concentration of traps and proportional to it $1/f$ noise exponentially grow with decreasing temperature in the variable range hopping regime. This theory provides smooth transition to the nearest neighbor hopping case where it predicts a very weak temperature dependence

The galactic population of white dwarfs

Original paper can be found at: http://www.iop.org/EJ/conf DOI: 10.1088/1742-6596/172/1/012004 [16th European White Dwarfs Workshop]The contribution of white dwarfs of the different Galactic populations to the stellar content of our Galaxy is only poorly known. Some authors claim a vast population of halo white dwarfs, which would be in accordance with some investigations of the early phases of Galaxy formation claiming a top-heavy initial– mass– function. Here, I present a model of the population of white dwarfs in the Milky Way based on observations of the local white dwarf sample and a standard model of Galactic structure. This model will be used to estimate the space densities of thin disc, thick disc and halo white dwarfs and their contribution to the baryonic mass budget of the Milky Way. One result of this investigation is that white dwarfs of the halo population contribute a large fraction of the Galactic white dwarf number count, but they are not responsible for the lion's share of stellar mass in the Milky Way. Another important result is the substantial contribution of the – often neglected – population of thick disc white dwarfs. Misclassification of thick disc white dwarfs is responsible for overestimates of the halo population in previous investigations.Peer reviewe

Genetic Contributions to Age-Related Decline in Executive Function: A 10-Year Longitudinal Study of COMT and BDNF Polymorphisms

Genetic variability in the dopaminergic and neurotrophic systems could contribute to age-related impairments in executive control and memory function. In this study we examined whether genetic polymorphisms for catechol-O-methyltransferase (COMT) and brain-derived neurotrophic factor (BDNF) were related to the trajectory of cognitive decline occurring over a 10-year period in older adults. A single nucleotide polymorphism in the COMT (Val158/108Met) gene affects the concentration of dopamine in the prefrontal cortex. In addition, a Val/Met substitution in the pro-domain for BDNF (Val66Met) affects the regulated secretion and trafficking of BDNF with Met carriers showing reduced secretion and poorer cognitive function. We found that impairments over the 10-year span on a task-switching paradigm did not vary as a function of the COMT polymorphism. However, for the BDNF polymorphism the Met carriers performed worse than Val homozygotes at the first testing session but only the Val homozygotes demonstrated a significant reduction in performance over the 10-year span. Our results argue that the COMT polymorphism does not affect the trajectory of age-related executive control decline, whereas the Val/Val polymorphism for BDNF may promote faster rates of cognitive decay in old age. These results are discussed in relation to the role of BDNF in senescence and the transforming impact of the Met allele on cognitive function in old age

The 3-phosphoinositide-dependent protein kinase 1 is an essential upstream activator of protein kinase A in malaria parasites

Cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) signalling is essential for the proliferation of Plasmodium falciparum malaria blood stage parasites. The mechanisms regulating the activity of the catalytic subunit PfPKAc, however, are only partially understood, and PfPKAc function has not been investigated in gametocytes, the sexual blood stage forms that are essential for malaria transmission. By studying a conditional PfPKAc knockdown (cKD) mutant, we confirm the essential role for PfPKAc in erythrocyte invasion by merozoites and show that PfPKAc is involved in regulating gametocyte deformability. We furthermore demonstrate that overexpression of PfPKAc is lethal and kills parasites at the early phase of schizogony. Strikingly, whole genome sequencing (WGS) of parasite mutants selected to tolerate increased PfPKAc expression levels identified missense mutations exclusively in the gene encoding the parasite orthologue of 3-phosphoinositide-dependent protein kinase-1 (PfPDK1). Using targeted mutagenesis, we demonstrate that PfPDK1 is required to activate PfPKAc and that T189 in the PfPKAc activation loop is the crucial target residue in this process. In summary, our results corroborate the importance of tight regulation of PfPKA signalling for parasite survival and imply that PfPDK1 acts as a crucial upstream regulator in this pathway and potential new drug target