Heterograft copolymers of poly(ε‐caprolactone) prepared by combination of ATRA “grafting onto” and ATRP “grafting from” processes

This paper aims at reporting on the synthesis of a heterograft copolymer by combining the “grafting onto” process based on atom transfer radical addition (ATRA) and the “grafting from” process by atom transfer radical polymerization (ATRP). The statistical copolymerization of ε‐caprolactone (εCL) and α‐chloro‐ε‐caprolactone (αClεCL) was initiated by 2,2‐dibutyl‐2‐stanna‐1,3‐dioxepane (DSDOP), followed by ATRA of parts of the chlorinated units of poly(αClεCL‐co‐εCL) on the terminal double bond of α‐MeO,ω‐CH₂?CH? CH₂? CO₂‐poly(ethylene oxide) (PEO). The amphiphilic poly(εCL‐g‐EO) graft copolymer collected at this stage forms micelles as supported by dynamic light scattering (DLS) and transmission electron microscopy (TEM). The unreacted pendant chloro groups of poly(εCL‐g‐EO) were used to initiate the ATRP of styrene with formation of copolymer with two populations of randomly distributed grafts, that is PEO and polystyrene. © 2006 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 44: 6015–6024, 2006     

Dynamic instabilities in scalar neural field equations with space-dependent delays

In this paper we consider a class of scalar integral equations with a form of space-dependent delay. These nonlocal models arise naturally when modelling neural tissue with active axons and passive dendrites. Such systems are known to support a dynamic (oscillatory) Turing instability of the homogeneous steady state. In this paper we develop a weakly nonlinear analysis of the travelling and standing waves that form beyond the point of instability. The appropriate amplitude equations are found to be the coupled mean-field Ginzburg-Landau equations describing a Turing-Hopf bifurcation with modulation group velocity of O(1). Importantly we are able to obtain the coefficients of terms in the amplitude equations in terms of integral transforms of the spatio-temporal kernels defining the neural field equation of interest. Indeed our results cover not only models with axonal or dendritic delays but also those which are described by a more general distribution of delayed spatio-temporal interactions. We illustrate the predictive power of this form of analysis with comparison against direct numerical simulations, paying particular attention to the competition between standing and travelling waves and the onset of Benjamin-Feir instabilities.     

Dynamic and redundant regulation of LRRK2 and LRRK1 expression

Background  

Mutations within the leucine-rich repeat kinase 2 (LRRK2) gene account for a significant proportion of autosomal-dominant and some late-onset sporadic Parkinson's disease. Elucidation of LRRK2 protein function in health and disease provides an opportunity for deciphering molecular pathways important in neurodegeneration. In mammals, LRRK1 and LRRK2 protein comprise a unique family encoding a GTPase domain that controls intrinsic kinase activity. The expression profiles of the murine LRRK proteins have not been fully described and insufficiently characterized antibodies have produced conflicting results in the literature.