So Far So Good: Emotion in the Peripersonal/Extrapersonal Space

Current accounts of spatial cognition and human-object interaction suggest that the representation of peripersonal space depends on an action-specific system that remaps its representation according to action requirements. Here we demonstrate that this mechanism is sensitive to knowledge about properties of objects. In two experiments we explored the interaction between physical distance and object attributes (functionality, desirability, graspability, etc.) through a reaching estimation task in which participants indicated if objects were near enough to be reached. Using both a real and a cutting-edge digital scenario, we demonstrate that perceived reaching distance is influenced by ease of grasp and the affective valence of an object. Objects with a positive affective valence tend to be perceived reachable at locations at which neutral or negative objects are perceived as non-reachable. In addition to this, reaction time to distant (non-reachable) positive objects suggests a bias to perceive positive objects as closer than negative and neutral objects (exp. 2). These results highlight the importance of the affective valence of objects in the action-specific mapping of the peripersonal/extrapersonal space system.     

Toxin-Antitoxin Genes of the Gram-Positive Pathogen Streptococcus pneumoniae: So Few and Yet So Many

Summary: Pneumococcal infections cause up to 2 million deaths annually and raise a large economic burden and thus constitute an important threat to mankind. Because of the increase in the antibiotic resistance of Streptococcus pneumoniae clinical isolates, there is an urgent need to find new antimicrobial approaches to triumph over pneumococcal infections. Toxin-antitoxin (TA) systems (TAS), which are present in most living bacteria but not in eukaryotes, have been proposed as an effective strategy to combat bacterial infections. Type II TAS comprise a stable toxin and a labile antitoxin that form an innocuous TA complex under normal conditions. Under stress conditions, TA synthesis will be triggered, resulting in the degradation of the labile antitoxin and the release of the toxin protein, which would poison the host cells. The three functional chromosomal TAS from S. pneumoniae that have been studied as well as their molecular characteristics are discussed in detail in this review. Furthermore, a meticulous bioinformatics search has been performed for 48 pneumococcal genomes that are found in public databases, and more putative TAS, homologous to well-characterized ones, have been revealed. Strikingly, several unusual putative TAS, in terms of components and genetic organizations previously not envisaged, have been discovered and are further discussed. Previously, we reported a novel finding in which a unique pneumococcal DNA signature, the BOX element, affected the regulation of the pneumococcal yefM-yoeB TAS. This BOX element has also been found in some of the other pneumococcal TAS. In this review, we also discuss possible relationships between some of the pneumococcal TAS with pathogenicity, competence, biofilm formation, persistence, and an interesting phenomenon called bistability.     

So Little Source, So Much Sink: Requirements for Afterdepolarizations to Propagate in Tissue

How early (EADs) and delayed afterdepolarizations (DADs) overcome electrotonic source-sink mismatches in tissue to trigger premature ventricular complexes remains incompletely understood. To study this question, we used a rabbit ventricular action potential model to simulate tissues in which a central area of contiguous myocytes susceptible to EADs or DADs was surrounded by unsusceptible tissue. In 1D tissue with normal longitudinal conduction velocity (0.55 m/s), the numbers of contiguous susceptible myocytes required for an EAD and a barely suprathreshold DAD to trigger a propagating action potential were 70 and 80, respectively. In 2D tissue, these numbers increased to 6940 and 7854, and in 3D tissue to 696,910 and 817,280. These numbers were significantly decreased by reduced gap junction conductance, simulated fibrosis, reduced repolarization reserve and heart failure electrical remodeling. In conclusion, the source-sink mismatch in well-coupled cardiac tissue powerfully protects the heart from arrhythmias due to sporadic afterdepolarizations. Structural and electrophysiological remodeling decrease these numbers significantly but still require synchronization mechanisms for EADs and DADs to overcome the robust protective effects of source-sink mismatch.