49 research outputs found
Optimal control theory based design of elasto-magnetic metamaterial
A method to design a new type of metamaterial is presented. A two-step strategy to define an optimal long-range force distribution embedded in an elastic support to control wave propagation is considered.
The first step uses a linear quadratic regulator (LQR) to produce an optimal set of long-range interactions. In the second step, a least square passive approximation of the LQR optimal gains is determined. The paper investigates numerical solutions obtained by the previously described procedure. Finally, we discuss physical and engineering implications and practical use of the present study
Twin-waves propagation phenomena in magnetically-coupled structures
The use of magnetic dipoles embedding in an elastic support introduces long-range interaction forces. This is a completely new paradigm in structural mechanics, classically based on local short-range particle interaction. The features of long-range forces produce very new mechanical coupling effects. This paper examines the case in which two identical rod-like structures, each with a dipole distribution embedded, vibrate side by side. Waves generated in one of the rods propagate also in the second and vice versa creating a new effect we name twin-waves. The present investigation unveils the existence of an infinite number of propagation modes even in one-dimensional infinite structures, a new and unus al behaviour in classical waveguides. The physics behind this phenomenon is further investigated also by numerical simulations
Long-range retarded elastic metamaterials: wave-stopping, negative, and hypersonic or superluminal group velocity
This paper investigates new phenomena in elastic wave propagation in metamaterials, characterised
by long-range interactions. The kind of waves borne in this context unveil wave-stopping,
negative group velocity, instability and hypersonic or superluminal effects, both for instantaneous
and for nonlocal retarded actions. Closed form results are presented and a universal propagation
map synthesizes the expected properties of these materials. Perspectives in physics, engineering and
social dynamics are discussed
Increased susceptibility to amyloid toxicity in familial Alzheimer's fibroblasts
Much experimental evidence suggests that an imbalance in cellular redox status is a major factor in the pathogenesis of Alzheimer's disease (AD). Our previous data showed a marked increase in membrane lipoperoxidation in primary fibroblasts from familial AD (FAD) patients. In the present study, we demonstrate that when oligomeric structures of A beta 1-40 and A beta 1-42 are added to the culture media, they accumulate quicker near the plasma membrane, and are internalized faster and mostly in APPV717I fibroblasts than in age-matched healthy cells; this results in an earlier and sharper increase in the production of reactive oxygen species (ROS). Higher ROS production leads in turn to an increase in membrane oxidative-injury and significant impairment of cellular antioxidant capacity, giving rise to apoptotic cascade activation and finally to a necrotic outcome. In contrast, healthy fibroblasts appear more resistant to amyloid oxidative-attack, possibly as a result of their plasma membrane integrity and powerful antioxidant capacity. Our data are consistent with increasing evidence that prefibrillar aggregates, compared to mature fibrils, are likely the more toxic species of the peptides. These findings provide compelling evidence that cells bearing increased membrane lipoperoxidation are more susceptible to aggregate toxicity as a result of their reduced ability to counteract amyloid oligomeric attack
Curcumin protects cardiac cells against ischemia-reperfusion injury: effects on oxidative stress, NF-kappaB, and JNK pathways
Seladin-1/dhcr24 protects neuroblastoma cells against aβ toxicity by increasing membrane cholesterol content
Linguistics
Contains table of contents for Section 4, an introduction and abstracts on seven doctoral dissertations
Losing Sight of Land: Tales of Dyslexia and Dyspraxia in Psychophysical Actor Training
This article reports on the findings of a research project into the impact of psychophysical actor training methods on neurodiverse students. It illustrates how the application of a Social Theory of Learning Difference reveals the mechanisms whereby these training methods dysconsciously discriminate against those students who are dyslexic and/or dyspraxic learners. The research findings recognise the inherent value of psychophysical methods in the training of actors but suggests that there is a need to move away from a singular Psycho-Medical Theory of Learning Difference and to adopt a framework of learning difference based on the Social Model of (dis)ability, which requires institutions to adapt their provision to better meet a diverse range of needs. A revision of psychophysical approaches is proposed, which draws on a neuroscientific theory of experiential practice and a psychological framework of actor engagement. This new approach seeks to enhance the effective communication of embodied knowledge and skills in diverse actor training contexts and to allow students who are dyslexic and/or dyspraxic learners equal access to that learning
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)
In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field