Collective Modes of Massive Dirac Fermions in Armchair Graphene Nanoribbons

We report the plasmon dispersion characteristics of intrinsic and extrinsic armchair graphene nanoribbons of atomic width N = 5 using a p_z-orbital tight binding model with third-nearest-neighbor (3nn) coupling. The coupling parameters are obtained by fitting the 3nn dispersions to that of an extended Huckel theory. The resultant massive Dirac Fermion system has a band gap E_g \approx 64 meV. The extrinsic plasmon dispersion relation is found to approach a common dispersion curve as the chemical potential $\mu$ increases, whereas the intrinsic plasmon dispersion relation is found to have both energy and momentum thresholds. We also report an analytical model for the extrinsic plasmon group velocity in the q \rightarrow 0 limit

Molecular Memory with Atomically-Smooth Graphene Contacts

We report the use of bilayer graphene as an atomically-smooth contact for nanoscale devices. A two-terminal Bucky ball (C60) based molecular memory is fabricated with bilayer graphene as a contact on the polycrystalline nickel electrode. Graphene provides an atomically-smooth covering over an otherwise rough metal surface. The use of graphene additionally prohibits the electromigration of nickel atoms into the C60 layer. The devices exhibit a low-resistance state in the first sweep cycle and irreversibly switch to a high resistance state at 0.8-1.2 V bias. The reverse sweep has a hysteresis behavior as well. In the subsequent cycles, the devices retain the high-resistance state, thus making it write-once read-many memory (WORM). The ratio of current in low-resistance to high-resistance state is lying in 20-40 range for various devices with excellent retention characteristics. Control sample without the bilayer graphene shows random hysteresis and switching.Comment: 13 pages and 4 figure

The ubiquity of state fragility : fault lines in the categorisation and conceptualisation of failed and fragile states

In the last three decades, the categories of fragile and failed states have gained significant importance in the fields of law, development, political science and international relations. The wider discourse plays a key role in guiding the policies of international community and multilateral institutions and has also led to the emergence of a plethora of indices and rankings to measure and classify state fragility. A critical and theoretical analysis of these matrices brings to light three crucial aspects that the current study takes as its departure point. First, the formulas and conceptual paradigms show that fragility of states is far more ubiquitous than is generally recognised, and that the so-called successful and stable states are a historical, political and geographical anomaly. Second, in the absence of an agreed definition of a successful state or even that of a failed or fragile state, the indicators generally rely on negative definitions to delineate the failed and fragile state. They generally suggest that their reading is built on a Weberian ideal–typical state, which takes the idea of monopoly over legitimate violence as its starting point. The third and final point suggests that the indicators and rankings, misconstruing the Weberian ideal–typical state, actually end up comparing fragile states against an ideal–mythical state. The article argues that this notional state is not only ahistorical and apolitical, but it also carries the same undertones that have been the hallmark of theories of linear development, colonialism and imperialism

Neuropathological investigations of three murine models of Huntington’s disease

Huntington’s disease (HD) is a purely genetic neurodegenerative disorder affecting approximately 1 in 10,000 people. It is most commonly associated with excessive involuntary movement, or chorea, combined with varying degrees of other motor, psychiatric and cognitive disturbances. Identification of the mutation in the HD gene prompted the generation of several transgenic mouse models. HD is but one of a family of at least 9 triplet repeat disorders, all of which exhibit protein aggregation by a similar mechanism. The understanding of one disease is therefore of importance to the understanding of them all. This thesis aims to be a comprehensive comparative study of three very different mouse models of HD elucidating the pathological changes that precede and accompany the disease process. The work described in this thesis presents a detailed account of a longitudinal study of the pathological changes that occur within the brains of founder generations of mice transgenic for exon 1 of the HD gene, containing a highly expanded CAG repeat, the R6 lines. I have determined the intracellular sites for deposition and accumulation of the mutant protein huntingtin (htt), within both the neurons and glia of the central nervous system. The progressive accumulation of additional proteins within these aggregates has been described. The temporal evolution and spatial distribution of the neuronal intranuclear inclusion (NII) was determined using both immunohistochemical and morphometric analyses. The cellular consequences resulting from the aggregation of mutant htt were also investigated. I have conducted a detailed morphometric analysis of neurones within the cerebral cortex, striatum and cerebellum throughout the period of protein deposition, until the eventual degeneration of these cells. The dendritic and somal changes resulting from the cellular disruption associated with these NII are also described. In a further series of experiments I have investigated the changes that occur in a novel model of HD, namely the conditional, doxycycline inducible double transgenic mouse, HD94 model. It was interesting to find that the same construct when differently manipulated in two mouse lines can produce such contrasting symptoms and pathology. This was highlighted by the comparison of immunohistochemical and morphometric analyses between the HD94 and the R6 lines, where the pattern of mutant protein deposition was found to vary significantly. Lastly I have studied a more genetically accurate murine model of HD, the HD80 ‘knock-in model’. These mice develop a pathology broadly similar to that of the R6 lines but markedly different to that of the HD94, and over a much longer time frame This detailed comparative analysis of the molecular and cellular pathology of three transgenic mouse models of HD provides new insights identifying novel and unique neuropathology and suggests new approaches for therapeutic treatments for this disease