The Egyptian Cardiothoracic Surgeon (ECTS - E-Journal)
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    Hybrid systems neuroscience

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    We define the field of hybrid systems neuroscience as the reformulation of hybrid system models, analysis tools and control schemes for neuronal systems. The field of hybrid systems has been built upon the theories of control and computer science. It has inherited control paradigms – including switching control systems and variable structure systems – originally designed for engineering problems, mainly in the areas of mechanical and electrical systems. The automated verification of hybrid systems has inherited computational paradigms originally designed for software systems or programs. The mixture has facilitated solutions to complex dynamical problems. However, the application of these paradigms to neuroscience cannot follow the orthodoxy of control and computational theories, and a new viewpoint isneeded to model and analyse the complex and unique behaviours of brain networks. Under the hybrid systems neuroscience framework, we propose new concepts like switching dominance, self-organising neuronal interdependent control (SONIC) or driver control neurons, and a new interpretation of hybrid automata. We illustrate these ideas in a novel working memory network model, which unifies the influence of dopamine, basal ganglia-thalamo-cortical circuits and the generation of subcortical background oscillations

    Zero-Bias Microwave Detectors Based on Array of Nanorectifiers Coupled with a Dipole Antenna

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    We report on zero-bias microwave detection using a large array of unipolar nanodevices, known as the self-switching diodes (SSDs). The large array was realized in a single lithography step without the need of interconnection layers, hence allowing for a simple and low-cost fabrication process. The SSD array was coupled with a narrowband dipole antenna with a resonant frequency of 890 MHz, to form a simple rectenna (rectifying antenna). The extrinsic voltage responsivity and noise-equivalent-power (NEP) of the rectenna were ∼70 V/W and ∼0.18 nW/Hz1/2, respectively, measured in the far-field region at unbiased condition. Nevertheless, the estimated intrinsic voltage responsivity can achieve up to ∼5 kV/W with NEP of ∼2.6 pW/Hz1/2

    'May depend on me sending it to you'::double objects in early grammars

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    In present-day standard English, verbs licensing two objects with a theme and a recipient usually allow for variation in word order between (1) I gave my sister a book, and (2) I gave a book to my sister. The former is considered the canonical word order: “[i]f both objects are present, the indirect object normally comes before” (Quirk et al. 1985:726), but with two pronominal objects the prepositional pattern like (2) is “by far the most frequent” variant (Biber et al. 1999:929). Historically, there has long been a third syntactic variant with a non-prepositional indirect object after the direct object: (3) she gave it me. With two pronominal objects this order “seems always to have been the rule” (Visser 1963:I.623), yet the sequence in (3) has gradually become restricted to linguistic contexts with two pronominal objects and to dialect use in certain varieties of British English (Yáñez-Bouza & Denison 2015). Denison (1998:239) observes that examples like (3) are “sufficient for that order to be accounted acceptable standard” in nineteenth-century English, while Poutsma (1914-1929:I.154) claims that in the early twentieth century “the indirect object almost invariably stands first,” and that with pronominal objects it is “not always” the case that the word order in (3) is preferred. The timing of change is crucial. The eighteenth and nineteenth centuries saw the publication of numerous grammars laying down rules about correct and incorrect English. Bearing in mind that normative rules have brought about change in the historical development of certain morphological and syntactic features, this paper aims to shed light on whether early grammarians were aware of syntactic variation in the double object construction, whether they were aware of regional variation, and whether they played a role in the suppression of variability concerning the pattern illustrated in (3)

    Radiation damage in biotite mica by accelerated α-particles: A synchrotron microfocus X-ray diffraction and X-ray absorption spectroscopy study

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    A critical radiation damage assessment of the materials that will be present in a Geological Disposal Facility (GDF) for radioactive waste is a priority for building a safety case. Detailed analysis of the effects of high-energy α-particle damage in phyllosilicates such as mica is a necessity, as these are model structures for both the clay-based backfill material and the highly sorbent components of a crystalline host rock. The α-radiation stability of biotite mica [general formula: K(Mg,Fe)3(Al,Si3O10)(F,OH)2] has been investigated using the 5 MV tandem pelletron at the University of Manchester’s Dalton Cumbrian Facility (DCF) and both the microfocus spectroscopy (I18) and core X-ray absorption spectroscopy (B18) beamlines at Diamond Light Source (U.K.). Microfocus X-ray diffraction mapping has demonstrated extensive structural aberrations in the mica resulting from controlled exposure to the focused 4He2+ ion (α-particle) beam. Delivered doses were comparable to a-particle fluences expected in the highly active, near-field of a GDF. At doses up to 6.77 displacements per atom (dpa) in the region of highest particle fluence, biotite mica displays a heterogeneous structural response to irradiation on a micrometer scale, with sequential dilation and contraction of regions of the structure perpendicular to the sheets, as well as a general overall contraction of the phyllosilicate layer spacing. At the peak of ion fluence, the structure collapses under a high point defect density and amorphous areas are pervasive among altered domains of the original lattice. Such structural alterations are likely to affect the material’s capacity to sorb and retain escaped radionuclides over long timescales; increased edge site availability may favor increased sorption while interlayer uptake will likely be reduced due to collapse. Radiation-induced reduction of structural iron at the region of highest structural damage across an α-particle’s track has been demonstrated by Fe K-edge X-ray absorption near edge spectroscopy (XANES) and local structural disorder has been confirmed by analysis of both potassium K-edge XANES and Fe K-edge extended X-ray absorption fine structure analysis. An infrared absorption study of deformations in the OH− stretching region, along with electron probe microanalysis complements the synchrotron data presented here

    Gene Cloning and DNA Analysis: An Introduction

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    Pathological tau deposition in Motor Neurone Disease and Frontotemporal Lobar Degeneration associated with TDP-43 proteinopathy

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    It has been suggested that patients with motor neurone disease (MND) and those with MND combined with behavioural variant frontotemporal dementia (bvFTD) (ie FTD + MND) or with FTD alone might exist on a continuum based on commonalities of neuropathology and/or genetic risk. Moreover, it has been reported that both a neuronal and a glial cell tauopathy can accompany the TDP-43 proteinopathy in patients with motor neurone disease (MND) with cognitive changes, and that the tauopathy may be fundamental to disease pathogenesis and clinical phenotype. In the present study, we sought to substantiate these latter findings, and test this concept of a pathological continuum, in a consecutive series of 41 patients with MND, 16 with FTD + MND and 23 with FTD without MND. Paraffin sections of frontal, entorhinal, temporal and occipital cortex and hippocampus were immunostained for tau pathology using anti-tau antibodies, AT8, pThr175 and pThr217, and for amyloid β protein (Aβ) using 4G8 antibody. Twenty four (59 %) patients with MND, 7 (44 %) patients with FTD + MND and 10 (43 %) patients with FTD showed ‘significant’ tau pathology (ie more than just an isolated neurofibrillary tangle or a few neuropil threads in one or more brain regions examined). In most instances, this bore the histological characteristics of an Alzheimer’s disease process involving entorhinal cortex, hippocampus, temporal cortex, frontal cortex and occipital cortex in decreasing frequency, accompanied by a deposition of Aβ up to Thal phase 3, though 2 patients with MND, and 1 with FTD did show tau pathology beyond Braak stage III. Four other patients with MND showed novel neuronal tau pathology, within the frontal cortex alone, specifically detected by pThr175 antibody, which was characterised by a fine granular or more clumped aggregation of tau without neurofibrillary tangles or neuropil threads. However, none of these 4 patients had clinically evident cognitive disorder, and this type of tau pathology was not seen in any of the FTD + MND or FTD patients. Finally, two patients, one with MND and one with FTD, showed a tau pathology consistent with Argyrophilic Grain Disease (AGD). Western blotting and use of 3- and 4-repeat tau antibodies confirmed the histological interpretation of Alzheimer’s disease type pathology in all instances except for those patients with accompanying AGD where a banding pattern on western blot, and immunohistochemistry, confirmed 4-repeat tauopathy. In all 3 patient groups, amyloid pathology was more likely to be present in patients dying after 65 years of age, and in the presence of APOE ε4 allele. We conclude that tau pathological changes are equally common amongst patients with MND, FTD + MND and FTD though, in most instances, these are limited in extent. In patients with MND, when cognitive impairment is present this is most likely due to an accompanying/evolving (coincidental) Alzheimer’s disease process or, as in a single case, Dementia with Lewy bodies, within the cerebral cortex rather than as a result of TDP-43 proteinopathy. Conversely, in FTD and FTD + MND dementia is more likely to be associated with TDP-43 proteinopathy than tau. Hence, present study shows no progression in severity of (tau) pathology from MND through FTD + MND to FTD, and does not support the concept of these conditions forming a continuum of clinical or pathological change

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