PTD4 Peptide Increases Neural Viability in an In Vitro Model of Acute Ischemic Stroke

Ischemic stroke is a disturbance in cerebral blood flow caused by brain tissue ischemia and hypoxia. We optimized a multifactorial in vitro model of acute ischemic stroke using rat primary neural cultures. This model was exploited to investigate the pro-viable activity of cell-penetrating peptides: arginine-rich Tat(49–57)-NH₂ (R⁴⁹KKRRQRRR⁵⁷-amide) and its less basic analogue, PTD4 (Y⁴⁷ARAAARQARA⁵⁷-amide). Our model included glucose deprivation, oxidative stress, lactic acidosis, and excitotoxicity. Neurotoxicity of these peptides was excluded below a concentration of 50 μm, and PTD4-induced pro-survival was more pronounced. Circular dichroism spectroscopy and molecular dynamics (MD) calculations proved potential contribution of the peptide conformational properties to neuroprotection: in MD, Tat(49–57)-NH₂ adopted a random coil and polyproline type II helical structure, whereas PTD4 adopted a helical structure. In an aqueous environment, the peptides mostly adopted a random coil conformation (PTD4) or a polyproline type II helical (Tat(49–57)-NH₂) structure. In 30% TFE, PTD4 showed a tendency to adopt a helical structure. Overall, the pro-viable activity of PTD4 was not correlated with the arginine content but rather with the peptide’s ability to adopt a helical structure in the membrane-mimicking environment, which enhances its cell membrane permeability. PTD4 may act as a leader sequence in novel drugs for the treatment of acute ischemic stroke.     

Negative recency and levels of processing in free recall.

Compared initial and final free recall of 5-item lists for 4 different "processing activities"; during list presentation 32 undergraduates either silently rehearsed, overtly rehearsed, generated rhymes, or generated verbal associates. Whereas the 2 rehearsal conditions showed a marked superiority in immediate free recall, their final (delayed) recall was inferior to that of lists for which associates were generated. It appears that the negative recency effect commonly obtained in delayed recall is a consequence of processing strategies which maximize the recency effect in immediate recall. (French summary) (17 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Two-step Prediction and Image Deflection for Exact Head Tracking in Virtual Environments

Time lag and image jittering are the main reasons for destroying the feeling of reality in most virtual environments. They cause motion sickness because human beings are simply not used to unrealistically generated feedback. This paper proposes advanced software methods that greatly reduce these unwanted effects: a new improved two-step prediction method for better head tracking, an image deflection technique to reduce remaining error and a new software configuration that allows the full use of available hardware capabilities. Our improved prediction technique reduces prediction error by 50% in comparison to standard methods. The image deflection allows to extend the prediction distance by 100% while keeping the error below a tolerable level.     

Impact of Polypyridyl Ru Complexes on Angiogenesis—Contribution to Their Antimetastatic Activity

The use of polypyridyl Ru complexes to inhibit metastasis is a novel approach, and recent studies have shown promising results. We have reported recently that Ru (II) complexes gathering two 4,7-diphenyl-1,10-phenanthroline (dip) ligands and the one being 2,2′-bipyridine (bpy) or its derivative with a 4-[3-(2-nitro-1H-imidazol-1-yl)propyl (bpy-NitroIm) or 5-(4-{4′-methyl-[2,2′-bipyridine]-4-yl}but-1-yn-1-yl)pyridine-2-carbaldehyde semicarbazone (bpy-SC) moieties can alter the metastatic cascade, among others, by modulating cell adhesion properties. In this work, we show further studies of this group of complexes by evaluating their effect on HMEC-1 endothelial cells. While all the tested complexes significantly inhibited the endothelial cell migration, Ru-bpy additionally interrupted the pseudovessels formation. Functional changes in endothelial cells might arise from the impact of the studied compounds on cell elasticity and expression of proteins (vinculin and paxillin) involved in focal adhesions. Furthermore, molecular studies showed that complexes modulate the expression of cell adhesion molecules, which has been suggested to be one of the factors that mediate the activation of angiogenesis. Based on the performed studies, we can conclude that the investigated polypyridyl Ru (II) complexes can deregulate the functionality of endothelial cells which may lead to the inhibition of angiogenesis.