Study Of Spatial Biological Systems Using a Graphical User Interface

Proceedings of the Tenth International Conference on Human-Computer Interaction, Crete, Greece, 22-27 June 2003In this paper, we describe a Graphical User Interface (GUI) designed to manage large quantities of image data of a biological system. After setting the design requirements for the system, we developed an ecology quantification GUI that assists biologists in analysing data. We focus on the main features of the interface and we present the results and an evaluation of the system. Finally, we provide some directions for some future work

The Effect of a Linear Tuning between the Antigenic Stimulations of CD4(+) T Cells and CD4(+) Tregs

We study the equilibria of an Ordinary Differencial Equation (ODE) system where CD4+ effector or helper T cells and Regulatory T cells (Tregs) are present. T cells trigger an immune response in the presence of their specific antigen. Regulatory T cells (Tregs) play a role in limiting auto-immune diseases due to their immune-suppressive ability. Here, we present explicit exact formulas that give the relationship between the concentration of T cells, the concentration of Tregs, and the antigenic stimulation of T cells, when the system is at equilibria, stable or unstable. We found a parameter region of bistability, limited by two thresholds of antigenic stimulation of T cells (hysteresis). Moreover, there are values of the slope parameter of the tuning for which an isola-center bifurcation appears, and, for some other values, there is a transcritical bifurcation. We also present time evolutions of the ODE system

Solar powered biohydrogen production requires specific localization of the hydrogenase

This work was supported by BBSRC Grant (BB/G021856/1) to SJB, PJN and CWM. We acknowledge support from the U.S. DoE, Biological and Environmental Research Program to MB, the U.S. DoE Fuel Cell Technologies Office (contract number DE-AC36-08-GO28308) to CAE and EPSRC (EP/F00270X/1) to MB and PJN

Supersymmetry Flows, Semi-Symmetric Space Sine-Gordon Models And The Pohlmeyer Reduction

We study the extended supersymmetric integrable hierarchy underlying the Pohlmeyer reduction of superstring sigma models on semi-symmetric superspaces F/G. This integrable hierarchy is constructed by coupling two copies of the homogeneous integrable hierarchy associated to the loop Lie superalgebra extension f of the Lie superalgebra f of F and this is done by means of the algebraic dressing technique and a Riemann-Hilbert factorization problem. By using the Drinfeld-Sokolov procedure we construct explicitly, a set of 2D spin \pm1/2 conserved supercharges generating supersymmetry flows in the phase space of the reduced model. We introduce the bi-Hamiltonian structure of the extended homogeneous hierarchy and show that the two brackets are of the Kostant-Kirillov type on the co-adjoint orbits defined by the light-cone Lax operators L_\pm. By using the second symplectic structure, we show that these supersymmetries are Hamiltonian flows, we compute part of the supercharge algebra and find the supersymmetric field variations they induce. We also show that this second Poisson structure coincides with the canonical Lorentz-Invariant symplectic structure of the WZNW model involved in the Lagrangian formulation of the extended integrable hierarchy, namely, the semi-symmetric space sine-Gordon model (SSSSG), which is the Pohlmeyer reduced action functional for the transverse degrees of freedom of superstring sigma models on the cosets F/G. We work out in some detail the Pohlmeyer reduction of the AdS_2xS^2 and the AdS_3xS^3 superstrings and show that the new conserved supercharges can be related to the supercharges extracted from 2D superspace. In particular, for the AdS_2xS^2 example, they are formally the same.Comment: V2: Two references added, V3: Modifications in section 2.6, V4: Published versio

Localisation and interactions of the Vipp1 protein in cyanobacteria

Biotechnology and Biological Sciences Research Council. Grant Number: BB/G021856. Deutsche Forschungsgemeinschaft. Grant Number: FOR 929, SCHN 690/3-1. European Commission. Grant Number: FP7-PEOPLE-2009-IEF 254575. NFR. Grant Numbers: 192436, 197119. OCISB. Royal Society and Engineering and Physical Sciences Research Council. Grant Number: EP/G0061009/

The AdS(5)xS(5) Semi-Symmetric Space Sine-Gordon Theory

The generalized symmetric space sine-Gordon theories are a series of 1+1-integrable field theories that are classically equivalent to superstrings on symmetric space spacetimes F/G. They are formulated in terms of a semi-symmetric space as a gauged WZW model with fermions and a potential term to deform it away from the conformal fixed point. We consider in particular the case of PSU(2,2|4)/Sp(2,2)xSp(4) which corresponds to AdS(5)xS(5). We argue that the infinite tower of conserved charges of these theories includes an exotic N=(8,8) supersymmetry that is realized in a mildy non-local way at the Lagrangian level. The supersymmetry is associated to a double central extension of the superalgebra psu(2|2)+psu(2|2) and includes a non-trivial R symmetry algebra corresponding to global gauge transformations, as well as 2-dimensional spacetime translations. We then explicitly construct soliton solutions and show that they carry an internal moduli superspace CP(2|1)xCP(2|1) with both bosonic and Grassmann collective coordinates. We show how to semi-classical quantize the solitons by writing an effective quantum mechanical system on the moduli space which takes the form of a co-adjoint orbit of SU(2|2)xSU(2|2). The spectrum consists of a tower of massive states in the short, or atypical, symmetric representations, just as the giant magnon states of the string world sheet theory, although here the tower is truncated.Comment: 39 pages, references adde

Fermionic Coset, Critical Level W^(2)_4-Algebra and Higher Spins

The fermionic coset is a limit of the pure spinor formulation of the AdS5xS5 sigma model as well as a limit of a nonlinear topological A-model, introduced by Berkovits. We study the latter, especially its symmetries, and map them to higher spin algebras. We show the following. The linear A-model possesses affine \AKMSA{pgl}{4}{4}_0 symmetry at critical level and its \AKMSA{psl}{4}{4}_0 current-current perturbation is the nonlinear model. We find that the perturbation preserves $\mathcal{W}^{(2)}_4$-algebra symmetry at critical level. There is a topological algebra associated to \AKMSA{pgl}{4}{4}_0 with the properties that the perturbation is BRST-exact. Further, the BRST-cohomology contains world-sheet supersymmetric symplectic fermions and the non-trivial generators of the $\mathcal{W}^{(2)}_4$-algebra. The Zhu functor maps the linear model to a higher spin theory. We analyze its \SLSA{psl}{4}{4} action and find finite dimensional short multiplets.Comment: 25 page

Tunable kinetic proofreading in a model with molecular frustration

In complex systems, feedback loops can build intricate emergent phenomena, so that a description of the whole system cannot be easily derived from the properties of the individual parts. Here we propose that inter-molecular frustration mechanisms can provide non trivial feedback loops which can develop nontrivial specificity amplification. We show that this mechanism can be seen as a more general form of a kinetic proofreading mechanism, with an interesting new property, namely the ability to tune the specificity amplification by changing the reactants concentrations. This contrasts with the classical kinetic proofreading mechanism in which specificity is a function of only the reaction rate constants involved in a chemical pathway. These results are also interesting because they show that a wide class of frustration models exists that share the same underlining kinetic proofreading mechanisms, with even richer properties. These models can find applications in different areas such as evolutionary biology, immunology and biochemistry

A Novel ZAP-70 Dependent FRET Based Biosensor Reveals Kinase Activity at both the Immunological Synapse and the Antisynapse

Many hypotheses attempting to explain the speed and sensitivity with which a T-cell discriminates the antigens it encounters include a notion of relative spatial and temporal control of particular biochemical steps involved in the process. An essential step in T-cell receptor (TCR) mediated signalling is the activation of the protein tyrosine kinase ZAP-70. ZAP-70 is recruited to the TCR upon receptor engagement and, once activated, is responsible for the phosphorylation of the protein adaptor, Linker for Activation of T-cells, or LAT. LAT phosphorylation results in the recruitment of a signalosome including PLCγ1, Grb2/SOS, GADS and SLP-76. In order to examine the real time spatial and temporal evolution of ZAP-70 activity following TCR engagement in the immune synapse, we have developed ROZA, a novel FRET-based biosensor whose function is dependent upon ZAP-70 activity. This new probe not only provides a measurement of the kinetics of ZAP-70 activity, but also reveals the subcellular localization of the activity as well. Unexpectedly, ZAP-70 dependent FRET was observed not only at the T-cell -APC interface, but also at the opposite pole of the cell or “antisynapse”

Kinesin expands and stabilizes the GDP-microtubule lattice

Kinesin-1 is a nanoscale molecular motor that walks towards the fast-growing (plus) ends of microtubules, hauling molecular cargo to specific reaction sites in cells. Kinesin-driven transport is central to the self-organization of eukaryotic cells and shows great promise as a tool for nano-engineering1. Recent work hints that kinesin may also play a role in modulating the stability of its microtubule track, both in vitro2,3 and in vivo4, but the results are conflicting5,6,7 and the mechanisms are unclear. Here, we report a new dimension to the kinesin–microtubule interaction, whereby strong-binding state (adenosine triphosphate (ATP)-bound and apo) kinesin-1 motor domains inhibit the shrinkage of guanosine diphosphate (GDP) microtubules by up to two orders of magnitude and expand their lattice spacing by ~1.6%. Our data reveal an unexpected mechanism by which the mechanochemical cycles of kinesin and tubulin interlock, and so allow motile kinesins to influence the structure, stability and mechanics of their microtubule track