Application of Design and Analysis of 23 Factorial experiment in determining some factors influencing recall ability in Short Term Memory

In this paper, we consider a 23 factorial experiment of factors influencing recall ability in short – term memory. The factors of interest are word length, word list and study time; and these factors tested on a group of students. The data obtained from the experiment are analyzed using the analysis of variance (ANOVA) of 23 factorial experiment (Yates Algorithm). The results show that recall ability in short term memory depends on word list, word length, study time and the interaction effect of list length and word length. Keywords: 23 factorial experiment, word length, design of experiment, Yate's Algorithm, Analysis of VarianceGlobal Journal of Pure and Applied Sciences Vol. 14 (3) 2008: pp. 371-37

Viscoelastic properties of differentiating blood cells are fate- and function-dependent

This is the final version of the article. Available from the publisher via the DOI in this record.Although cellular mechanical properties are known to alter during stem cell differentiation, understanding of the functional relevance of such alterations is incomplete. Here, we show that during the course of differentiation of human myeloid precursor cells into three different lineages, the cells alter their viscoelastic properties, measured using an optical stretcher, to suit their ultimate fate and function. Myeloid cells circulating in blood have to be advected through constrictions in blood vessels, engendering the need for compliance at short time-scales (minutes), compared to undifferentiated cells. These findings suggest that reduction in steady-state viscosity is a physiological adaptation for enhanced migration through tissues. Our results indicate that the material properties of cells define their function, can be used as a cell differentiation marker and could serve as target for novel therapies.Funding: The authors acknowledge financial support by the Cambridge Commonwealth Trust (to AEE; http://www.cambridgetrusts.org), the Medical Research Council (to KC and JG; grant number: 94185; http://www.mrc.ac.uk), the Human Frontier Science Program (to GW and JG; grant number: RGP0015/2009-C; http:// www.hfsp.org) and the European Research Council (to JG; grant number: 282060; http://erc.europa.eu)

Mechanical deformation induces depolarization of neutrophils

The transition of neutrophils from a resting state to a primed state is an essential requirement for their function as competent immune cells. This transition can be caused not only by chemical signals but also by mechanical perturbation. After cessation of either, these cells gradually revert to a quiescent state over 40 to 120 min. We use two biophysical tools, an optical stretcher and a novel microcirculation mimetic, to effect physiologically relevant mechanical deformations of single nonadherent human neutrophils. We establish quantitative morphological analysis and mechanical phenotyping as label-free markers of neutrophil priming. We show that continued mechanical deformation of primed cells can cause active depolarization, which occurs two orders of magnitude faster than by spontaneous depriming. This work provides a cellular-level mechanism that potentially explains recent clinical studies demonstrating the potential importance, and physiological role, of neutrophil depriming in vivo and the pathophysiological implications when this deactivation is impaired, especially in disorders such as acute lung injury.We acknowledge financial support by the Cambridge Commonwealth Trust (to A.E.E.), the European Research Council (Starting Grant “Light Touch” to J.G.), and the National Institute for Health Research Cambridge Biomedical Research Centre (to E.R.C.). C.S. is a Wellcome Trust Postdoctoral Clinical Research Fellow (101692MA), and C.F. is a Medical Research Council Clinical Training Fellow

Towards Securing the Home Computer: a modification of the USB Port

Hundreds of millions of people use the home computer everyday for different purposes. These systems use the universal serial bus (USB) disk for day to day transfer of data, communication and other applications. The USB as a flexible tool for data transfer raises security concerns relatively to a potential loss of assets. This paper therefore demonstrates how a modification of the USB port can improve the security of the home computer.Keywords: home computer, operating system, threats, Universal Serial Bus (USB)Journal of the Nigerian Association of Mathematical Physics, Volume 20 (March, 2012), pp 461 – 46

Towards Securing the Home Computer: a modification of the USB Port

Hundreds of millions of people use the home computer everyday for different purposes. These systems use the universal serial bus (USB) disk for day to day transfer of data, communication and other applications. The USB as a flexible tool for data transfer raises security concerns relatively to a potential loss of assets. This paper therefore demonstrates how a modification of the USB port can improve the security of the home computer.Keywords: home computer, operating system, threats, Universal Serial Bus (USB)

Amelioration of age-related brain function decline by Bruton's tyrosine kinase inhibition

One of the hallmarks of aging is the progressive accumulation of senescent cells in organisms, which has been proposed to be a contributing factor to age-dependent organ dysfunction. We recently reported that Bruton's tyrosine kinase (BTK) is an upstream component of the p53 responses to DNA damage. BTK binds to and phosphorylates p53 and MDM2, which results in increased p53 activity. Consistent with this, blocking BTK impairs p53-induced senescence. This suggests that sustained BTK inhibition could have an effect on organismal aging by reducing the presence of senescent cells in tissues. Here, we show that ibrutinib, a clinically approved covalent inhibitor of BTK, prolonged the maximum lifespan of a Zmpste24−/− progeroid mice, which also showed a reduction in general age-related fitness loss. Importantly, we found that certain brain functions were preserved, as seen by reduced anxiety-like behaviour and better long-term spatial memory. This was concomitant to a decrease in the expression of specific markers of senescence in the brain, which confirms a lower accumulation of senescent cells after BTK inhibition. Our data show that blocking BTK has a modest increase in lifespan in Zmpste24−/− mice and protects them from a decline in brain performance. This suggests that specific inhibitors could be used in humans to treat progeroid syndromes and prevent the age-related degeneration of organs such as the brain

Detecting and targeting senescent cells using molecularly imprinted nanoparticles

The progressive accumulation of senescent cells in tissues in response to damage importantly contributes to pathophysiological conditions such as fibrosis, diabetes, cancer, Alzheimer's and ageing. Consistent with this, eliminating senescent cells prolongs the lifespan and healthspan in animals and ameliorates certain diseases. Detecting and clearing senescent cells from human tissues could therefore have a significant diagnostic and prognostic impact. However, identifying senescent cells in vivo has proven to be complex. To address this, we characterized and validated a panel of novel membrane markers of senescence. Here, we show the application of molecularly imprinted nanoparticles (nanoMIPs) against an extracellular epitope of one of these markers, B2M, to detect senescent cells in vitro and in vivo. We show that nanoMIPs do not elicit toxic responses in the cells or in mice and successfully recognize old animals, which have a higher proportion of senescent cells in their organs. Importantly, nanoMIPs loaded with drugs can specifically kill senescent cells. Our results provide a proof-of-principle assessment of specific and safe nanotechnology-based approaches for senescent cell detection and clearance with potential clinical relevance