Stress impairs intentional memory control through altered theta oscillations in lateral parietal cortex

Accumulating evidence suggests that forgetting is not necessarily a passive process but that we can, to some extent, actively control what we remember and what we forget. Although this intentional control of memory has potentially far-reaching implications, the factors that influence our capacity to intentionally control our memory are largely unknown. Here, we tested whether acute stress may disrupt the intentional control of memory and, if so, through which neural mechanism. We exposed healthy men and women to a stress (n=27) or control (n=26) procedure before they aimed repeatedly to retrieve some previously learned cue-target pairs and to actively suppress others. While control participants showed reduced memory for supressed compared to baseline pairs in a subsequent memory test, this suppression-induced forgetting was completely abolished after stress. Using magnetoencephalography (MEG), we show that the reduced ability to suppress memories after stress is associated with altered theta activity in the inferior temporal cortex when the control process (retrieval or suppression) is triggered and in the lateral parietal cortex when control is exerted, with the latter being directly correlated with the stress hormone cortisol. Moreover, the suppression-induced forgetting was linked to altered connectivity between the hippocampus and right dorsolateral prefrontal cortex, which in turn was negatively correlated to stress-induced cortisol increases. These findings provide novel insights into conditions under which our capacity to actively control our memory breaks down and may have considerable implications for stress-related psychopathologies, such as posttraumatic stress disorder, that are characterized by unwanted memories of distressing events.Significance Statement: It is typically assumed that forgetting is a passive process that can hardly be controlled. There is, however, evidence that we may actively control, to some extent, what we remember and what we forget. This intentional memory control has considerable implications for mental disorders in which patients suffer from unwanted (e.g., traumatic) memories. Here, we demonstrate that the capacity to intentionally control our memory breaks down after stress. Using magnetoencephalography, we show that this stress-induced memory control deficit is linked to altered activity in the lateral parietal cortex and the connectivity between the hippocampus and right prefrontal cortex. These findings provide novel insights into conditions under which memory control fails and are highly relevant in the context of stress-related psychopathologies

Induction of leaf senescence in Arabidopsis thaliana by long days through a light-dosage effect

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/74662/1/j.1399-3054.1996.tb00463.x.pd

Quantum theory of electromechanical noise and momentum transfer statistics

A quantum mechanical theory is developed for the statistics of momentum transferred to the lattice by conduction electrons. Results for the electromechanical noise power in the semiclassical diffusive transport regime agree with a recent theory based on the Boltzmann-Langevin equation. All moments of the transferred momentum are calculated for a single-channel conductor with a localized scatterer, and compared with the known statistics of transmitted charge.Comment: 10 pages, 2 figure

The structure of the core NuRD repression complex provides insights into its interaction with chromatin

The NuRD complex is a multi-protein transcriptional corepressor that couples histone deacetylase and ATP-dependent chromatin remodelling activities. The complex regulates the higher-order structure of chromatin, and has important roles in the regulation of gene expression, DNA damage repair and cell differentiation. HDACs 1 and 2 are recruited by the MTA1 corepressor to form the catalytic core of the complex. The histone chaperone protein RBBP4, has previously been shown to bind to the carboxy-terminal tail of MTA1. We show that MTA1 recruits a second copy of RBBP4. The crystal structure reveals an extensive interface between MTA1 and RBBP4. An EM structure, supported by SAXS and crosslinking, reveals the architecture of the dimeric HDAC1:MTA1:RBBP4 assembly which forms the core of the NuRD complex. We find evidence that in this complex RBBP4 mediates interaction with histone H3 tails, but not histone H4, suggesting a mechanism for recruitment of the NuRD complex to chromati

Stress fracture of the thoracic spine in a male rugby player: a case report

This case reports a stress fracture of the thoracic spine in a professional rugby player. This is a rare anatomical location for this type of injury in this population and has not previously been described. Physicians should be aware that performance of rugby specific movements may lead to rare stress fractures in certain anatomic locations

Estrogen receptor transcription and transactivation: Structure-function relationship in DNA- and ligand-binding domains of estrogen receptors

Estrogen receptors are members of the nuclear receptor steroid family that exhibit specific structural features, ligand-binding domain sequence identity and dimeric interactions, that single them out. The crystal structures of their DNA-binding domains give some insight into how nuclear receptors discriminate between DNA response elements. The various ligand-binding domain crystal structures of the two known estrogen receptor isotypes (α and β) allow one to interpret ligand specificity and reveal the interactions responsible for stabilizing the activation helix H12 in the agonist and antagonist positions

The Ruderman-Kittel-Kasuya-Yosida (RKKY) interaction across a tunneling junction out of equilibrium

The Ruderman-Kittel-Kasuya-Yosida (RKKY) interaction between two magnetic $s$-$d$ spin impurities across a tunneling junction is studied when the system is driven out of equilibrium through biasing the junction. The nonequilibrium situation is handled with the Keldysh time-loop perturbation formalism in conjunction with appropriate coupling methods for tunneling systems due to Caroli and Feuchtwang. We find that the presence of a nonequilibrium bias across the junction leads to an interference of several fundamental oscillations, such that in this tunneling geometry, it is possible to tune the interaction between ferromagnetic and antiferromagnetic coupling at a fixed impurity configuration, simply by changing the bias across the junction. Furthermore, it is shown that the range of the RKKY interaction is altered out of equilibrium, such that in particular the interaction energy between two slabs of spins scales extensively with the thickness of the slabs in the presence of an applied bias.Comment: 38 pages revtex preprint; 5 postscript figures; submitted to Phys. Rev.

Projecting Pharmaceutical Expenditure in EU5 to 2021: Adjusting for the Impact of Discounts and Rebates

Within (European) healthcare systems, the main goal for pharmaceutical expenditure is cost containment. This is due to a general belief among healthcare policy makers that pharmaceutical expenditure—driven by high prices—will be unsustainable unless further reforms are enacted.The aim of the research published in this paper is to provide more realistic expectations of pharmaceutical expenditure for all key stakeholder groups by estimating pharmaceutical expenditure at ‘net’ prices. We also aim to estimate any gaps developing between list and net pharmaceutical expenditure for the EU5 countries (i.e. France, Germany, Italy, Spain, and the UK). We adjusted an established forecast of pharmaceutical expenditure for the EU5 countries, from 2017 to 2021, by reflecting discounts and rebates not previously considered, i.e. we moved from ‘list’ to ‘net’ prices, as far as data were available.We found an increasing divergence between expenditure measured at list and net prices. When the forecasts for the five countries were aggregated, the EU5 (unweighted) average historical growth (2010–2016) rate fell from 3.4% compound annual growth rate at list to 2.5% at net. For the forecast, the net growth rate was estimated at 1.5 versus 2.9% at list.Our results suggest that future growth in pharmaceutical expenditure in Europe is likely to be (1) lower than previously understood from forecasts based on list prices and (2) below predicted healthcare expenditure growth in Europe and in line with long-term economic growth rates. For policy makers concerned about the sustainability of pharmaceutical expenditure, this study may provide some comfort, in that the perceived problem is not as large as expected