The electrical and optical properties of zinc suphide platelets

Imperial Users onl

Watching the savages dance : problems and possibilities of creating post-colonial performance in a bi-cultural country

This thesis will examine the question of how to perform the cultural Other in New Zealand, utilising Daniel Defoe's Robinson Crusoe as the text for performance. This text provides a relevance to New Zealand through various similarities between the novel and this country, in particular articulating a paradigmatic Self/Other relationship between the figure of Crusoe and the primitive savages which can be employed to interrogate New Zealand's own colonial history. The inquiry into the performance of Robinson Crusoe has been the primary focus of a group of post-graduate students of the Theatre and Film Studies Department at University of Canterbury, since an initial performance of Robinson Crusoe in 1996. The question of how to perform the Other is particularised by the cultural specificity of the group, which is ideologically entirely pakeha. This question thus becomes a political issue of whether or not a pakeha group can perform a Maori Other. Through the question being postulated under the auspices of performance, the key scene from the Defoe text in which Crusoe watches the savages dance will provide a concrete model with which to constantly engage. This scene will be examined in both chapters, utilised in the first chapter as a means to enter into an analysis of the perception of the Other, and being considered in terms of theatricality in Chapter Two. Ultimately it would appear that to perform Otherness, or to perform Maori-ness, is impossible, due to the perception that every move a pakeha group makes towards this performance is perceived as culturally loaded. Nevertheless, I propose that it is a worthwhile and necessary endeavour to attempt such a performance of the Other, for this will at least raise questions rather than leave things in a state of conjecture

A new look at sodium channel β subunits.

Voltage-gated sodium (Nav) channels are intrinsic plasma membrane proteins that initiate the action potential in electrically excitable cells. They are a major focus of research in neurobiology, structural biology, membrane biology and pharmacology. Mutations in Nav channels are implicated in a wide variety of inherited pathologies, including cardiac conduction diseases, myotonic conditions, epilepsy and chronic pain syndromes. Drugs active against Nav channels are used as local anaesthetics, anti-arrhythmics, analgesics and anti-convulsants. The Nav channels are composed of a pore-forming α subunit and associated β subunits. The β subunits are members of the immunoglobulin (Ig) domain family of cell-adhesion molecules. They modulate multiple aspects of Nav channel behaviour and play critical roles in controlling neuronal excitability. The recently published atomic resolution structures of the human β3 and β4 subunit Ig domains open a new chapter in the study of these molecules. In particular, the discovery that β3 subunits form trimers suggests that Nav channel oligomerization may contribute to the functional properties of some β subunits

Post-translational modifications of voltage-gated sodium channels in chronic pain syndromes.

In the peripheral sensory nervous system the neuronal expression of voltage-gated sodium channels (Navs) is very important for the transmission of nociceptive information since they give rise to the upstroke of the action potential (AP). Navs are composed of nine different isoforms with distinct biophysical properties. Studying the mutations associated with the increase or absence of pain sensitivity in humans, as well as other expression studies, have highlighted Nav1.7, Nav1.8, and Nav1.9 as being the most important contributors to the control of nociceptive neuronal electrogenesis. Modulating their expression and/or function can impact the shape of the AP and consequently modify nociceptive transmission, a process that is observed in persistent pain conditions. Post-translational modification (PTM) of Navs is a well-known process that modifies their expression and function. In chronic pain syndromes, the release of inflammatory molecules into the direct environment of dorsal root ganglia (DRG) sensory neurons leads to an abnormal activation of enzymes that induce Navs PTM. The addition of small molecules, i.e., peptides, phosphoryl groups, ubiquitin moieties and/or carbohydrates, can modify the function of Navs in two different ways: via direct physical interference with Nav gating, or via the control of Nav trafficking. Both mechanisms have a profound impact on neuronal excitability. In this review we will discuss the role of Protein Kinase A, B, and C, Mitogen Activated Protein Kinases and Ca++/Calmodulin-dependent Kinase II in peripheral chronic pain syndromes. We will also discuss more recent findings that the ubiquitination of Nav1.7 by Nedd4-2 and the effect of methylglyoxal on Nav1.8 are also implicated in the development of experimental neuropathic pain. We will address the potential roles of other PTMs in chronic pain and highlight the need for further investigation of PTMs of Navs in order to develop new pharmacological tools to alleviate pain

The Voltage-Dependent Sodium Channel Family.

In neurones and other electrically excitable tissues, voltage-dependent sodium (Nav) channels play an essential role in initiating and propagating the action potential. High-resolution structures of sodium channels have revealed new details concerning these macromolecules that provide insights into their ion-specificity and the conformational changes they undergo during the action potential. Nav channels typically exist in vivo as multicomponent macromolecular assemblies, containing auxiliary proteins that modulate channel gating and trafficking. The properties of some of these auxiliary proteins raise the possibility that Nav channels may exist as functionally coupled complexes. The close similarity between different Nav channel subtypes has frustrated attempts to develop isoform-specific inhibitors. However, the combination of new structural insights, together with antibody-based reagents and site-directed mutagenesis of protein-based toxin inhibitors, raises the possibility of higher target specificities than previously possible. Such reagents may form the basis for a new generation of Nav channel drugs

Review and Unification of Methods for Computing Derivatives of Multidisciplinary Systems

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/97061/1/AIAA2012-1589.pd

Automatic sensitivity code for computational fluid dynamics

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