Concept and Mathematical Modeling of Acoustic Emission Source

Presently, most acoustic emission applications in nondestructive testing involve placing transducers on a large structure, a bridge or hydrocarbon cracking pressure vessel, then loading the structure and listening for the burst-type acoustic emissions that ensue, and ,finally using triangulation to locate the flaws whence came those bursts. This technique is very effective at locating defects, and that means that the typical, most studied acoustic emission parameters are just the number of events, the event rate, and to a somewhat lesser extent, the maximum amplitude . It might be the root mean square. amplitude, or some other amplitude that characterizes the acoustic emission, or an amplitude distribution, that is, the number greater than some threshold V. These are typical, widely used acoustic emission parameters, and they have been very successful in locating defects. In fact, if they hadn\u27t been, I don\u27t think I would be here today talking about fancier things in acoustic emission

Shape Changes of Self-Assembled Actin Bilayer Composite Membranes

We report the self-assembly of thin actin shells beneath the membranes of giant vesicles. Ion-carrier mediated influx of Mg2+ induces actin polymerization in the initially spherical vesicles. Buckling of the vesicles and the formation of blisters after thermally induced bilayer expansion is demonstrated. Bilayer flickering is dominated by tension generated by its coupling to the actin cortex. Quantitative flicker analysis suggests the bilayer and the actin cortex are separated by 0.4 \mum to 0.5 \mum due to undulation forces.Comment: pdf-file, has been accepted by PR

Short-time inertial response of viscoelastic fluids measured with Brownian motion and with active probes

We have directly observed short-time stress propagation in viscoelastic fluids using two optically trapped particles and a fast interferometric particle-tracking technique. We have done this both by recording correlations in the thermal motion of the particles and by measuring the response of one particle to the actively oscillated second particle. Both methods detect the vortex-like flow patterns associated with stress propagation in fluids. This inertial vortex flow propagates diffusively for simple liquids, while for viscoelastic solutions the pattern spreads super-diffusively, dependent on the shear modulus of the medium

Achieving Optimal Growth through Product Feedback Inhibition in Metabolism

Recent evidence suggests that the metabolism of some organisms, such as Escherichia coli, is remarkably efficient, producing close to the maximum amount of biomass per unit of nutrient consumed. This observation raises the question of what regulatory mechanisms enable such efficiency. Here, we propose that simple product-feedback inhibition by itself is capable of leading to such optimality. We analyze several representative metabolic modules—starting from a linear pathway and advancing to a bidirectional pathway and metabolic cycle, and finally to integration of two different nutrient inputs. In each case, our mathematical analysis shows that product-feedback inhibition is not only homeostatic but also, with appropriate feedback connections, can minimize futile cycling and optimize fluxes. However, the effectiveness of simple product-feedback inhibition comes at the cost of high levels of some metabolite pools, potentially associated with toxicity and osmotic imbalance. These large metabolite pool sizes can be restricted if feedback inhibition is ultrasensitive. Indeed, the multi-layer regulation of metabolism by control of enzyme expression, enzyme covalent modification, and allostery is expected to result in such ultrasensitive feedbacks. To experimentally test whether the qualitative predictions from our analysis of feedback inhibition apply to metabolic modules beyond linear pathways, we examine the case of nitrogen assimilation in E. coli, which involves both nutrient integration and a metabolic cycle. We find that the feedback regulation scheme suggested by our mathematical analysis closely aligns with the actual regulation of the network and is sufficient to explain much of the dynamical behavior of relevant metabolite pool sizes in nutrient-switching experiments

Characterization of Engineered Actin Binding Proteins That Control Filament Assembly and Structure

Eukaryotic cells strictly regulate the structure and assembly of their actin filament networks in response to various stimuli. The actin binding proteins that control filament assembly are therefore attractive targets for those who wish to reorganize actin filaments and reengineer the cytoskeleton. Unfortunately, the naturally occurring actin binding proteins include only a limited set of pointed-end cappers, or proteins that will block polymerization from the slow-growing end of actin filaments. Of the few that are known, most are part of large multimeric complexes that are challenging to manipulate.We describe here the use of phage display mutagenesis to generate of a new class of binding protein that can be targeted to the pointed-end of actin. These proteins, called synthetic antigen binders (sABs), are based on an antibody-like scaffold where sequence diversity is introduced into the binding loops using a novel "reduced genetic code" phage display library. We describe effective strategies to select and screen for sABs that ensure the generated sABs bind to the pointed-end surface of actin exclusively.From our set of pointed-end binders, we identify three sABs with particularly useful properties to systematically probe actin dynamics: one protein that caps the pointed end, a second that crosslinks actin filaments, and a third that severs actin filaments and promotes disassembly

Protein Evolution by Molecular Tinkering: Diversification of the Nuclear Receptor Superfamily from a Ligand-Dependent Ancestor

Phylogenetic reconstruction of the structure and function of the ancestor of the nuclear receptor protein family reveals how functional diversity evolves by subtle tinkering with an ancestral template

Tension and Robustness in Multitasking Cellular Networks

Cellular networks multitask by exhibiting distinct, context-dependent dynamics. However, network states (parameters) that generate a particular dynamic are often sub-optimal for others, defining a source of “tension” between them. Though multitasking is pervasive, it is not clear where tension arises, what consequences it has, and how it is resolved. We developed a generic computational framework to examine the source and consequences of tension between pairs of dynamics exhibited by the well-studied RB-E2F switch regulating cell cycle entry. We found that tension arose from task-dependent shifts in parameters associated with network modules. Although parameter sets common to distinct dynamics did exist, tension reduced both their accessibility and resilience to perturbation, indicating a trade-off between “one-size-fits-all” solutions and robustness. With high tension, robustness can be preserved by dynamic shifting of modules, enabling the network to toggle between tasks, and by increasing network complexity, in this case by gene duplication. We propose that tension is a general constraint on the architecture and operation of multitasking biological networks. To this end, our work provides a framework to quantify the extent of tension between any network dynamics and how it affects network robustness. Such analysis would suggest new ways to interfere with network elements to elucidate the design principles of cellular networks

Use of television, videogames, and computer among children and adolescents in Italy

<p>Abstract</p> <p>Background</p> <p>This survey determined the practices about television (video inclusive), videogames, and computer use in children and adolescents in Italy.</p> <p>Methods</p> <p>A self-administered anonymous questionnaire covered socio-demographics; behaviour about television, videogames, computer, and sports; parental control over television, videogames, and computer.</p> <p>Results</p> <p>Overall, 54.1% and 61% always ate lunch or dinner in front of the television, 89.5% had a television in the bedroom while 52.5% of them always watched television there, and 49% indicated that parents controlled the content of what was watched on television. The overall mean length of time daily spent on television viewing (2.8 hours) and the frequency of watching for at least two hours per day (74.9%) were significantly associated with older age, always ate lunch or dinner while watching television, spent more time playing videogames and using computer. Those with parents from a lower socio-economic level were also more likely to spend more minutes viewing television. Two-thirds played videogames for 1.6 daily hours and more time was spent by those younger, males, with parents that do not control them, who watched more television, and who spent more time at the computer. The computer was used by 85% of the sample for 1.6 daily hours and those older, with a computer in the bedroom, with a higher number of computers in home, who view more television and play videogames were more likely to use the computer.</p> <p>Conclusion</p> <p>Immediate and comprehensive actions are needed in order to diminish time spent at the television, videogames, and computer.</p

A Systematic Analysis of Cell Cycle Regulators in Yeast Reveals That Most Factors Act Independently of Cell Size to Control Initiation of Division

Upstream events that trigger initiation of cell division, at a point called START in yeast, determine the overall rates of cell proliferation. The identity and complete sequence of those events remain unknown. Previous studies relied mainly on cell size changes to identify systematically genes required for the timely completion of START. Here, we evaluated panels of non-essential single gene deletion strains for altered DNA content by flow cytometry. This analysis revealed that most gene deletions that altered cell cycle progression did not change cell size. Our results highlight a strong requirement for ribosomal biogenesis and protein synthesis for initiation of cell division. We also identified numerous factors that have not been previously implicated in cell cycle control mechanisms. We found that CBS, which catalyzes the synthesis of cystathionine from serine and homocysteine, advances START in two ways: by promoting cell growth, which requires CBS's catalytic activity, and by a separate function, which does not require CBS's catalytic activity. CBS defects cause disease in humans, and in animals CBS has vital, non-catalytic, unknown roles. Hence, our results may be relevant for human biology. Taken together, these findings significantly expand the range of factors required for the timely initiation of cell division. The systematic identification of non-essential regulators of cell division we describe will be a valuable resource for analysis of cell cycle progression in yeast and other organisms

Evidence for the Complexity of MicroRNA-Mediated Regulation in Ovarian Cancer: A Systems Approach

MicroRNAs (miRNAs) are short (∼22 nucleotides) regulatory RNAs that can modulate gene expression and are aberrantly expressed in many diseases including cancer. Previous studies have shown that miRNAs inhibit the translation and facilitate the degradation of their targeted messenger RNAs (mRNAs) making them attractive candidates for use in cancer therapy. However, the potential clinical utility of miRNAs in cancer therapy rests heavily upon our ability to understand and accurately predict the consequences of fluctuations in levels of miRNAs within the context of complex tumor cells. To evaluate the predictive power of current models, levels of miRNAs and their targeted mRNAs were measured in laser captured micro-dissected (LCM) ovarian cancer epithelial cells (CEPI) and compared with levels present in ovarian surface epithelial cells (OSE). We found that the predicted inverse correlation between changes in levels of miRNAs and levels of their mRNA targets held for only ∼11% of predicted target mRNAs. We demonstrate that this low inverse correlation between changes in levels of miRNAs and their target mRNAs in vivo is not merely an artifact of inaccurate miRNA target predictions but the likely consequence of indirect cellular processes that modulate the regulatory effects of miRNAs in vivo. Our findings underscore the complexities of miRNA-mediated regulation in vivo and the necessity of understanding the basis of these complexities in cancer cells before the therapeutic potential of miRNAs can be fully realized