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      On-site Rapid Diagnosis of Intracranial Hematoma using Portable Multi-slice Microwave Imaging System

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      a , 1 , 1
      Scientific Reports
      Nature Publishing Group

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          Abstract

          Rapid, on-the-spot diagnostic and monitoring systems are vital for the survival of patients with intracranial hematoma, as their conditions drastically deteriorate with time. To address the limited accessibility, high costs and static structure of currently used MRI and CT scanners, a portable non-invasive multi-slice microwave imaging system is presented for accurate 3D localization of hematoma inside human head. This diagnostic system provides fast data acquisition and imaging compared to the existing systems by means of a compact array of low-profile, unidirectional antennas with wideband operation. The 3D printed low-cost and portable system can be installed in an ambulance for rapid on-site diagnosis by paramedics. In this paper, the multi-slice head imaging system’s operating principle is numerically analysed and experimentally validated on realistic head phantoms. Quantitative analyses demonstrate that the multi-slice head imaging system is able to generate better quality reconstructed images providing 70% higher average signal to clutter ratio, 25% enhanced maximum signal to clutter ratio and with around 60% hematoma target localization compared to the previous head imaging systems. Nevertheless, numerical and experimental results demonstrate that previous reported 2D imaging systems are vulnerable to localization error, which is overcome in the presented multi-slice 3D imaging system. The non-ionizing system, which uses safe levels of very low microwave power, is also tested on human subjects. Results of realistic phantom and subjects demonstrate the feasibility of the system in future preclinical trials.

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          Most cited references22

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          Intracerebral haemorrhage (ICH) is the most devastating type of stroke and is a leading cause of disability and mortality. By contrast with advances in ischaemic stroke treatment, few evidence-based targeted treatments exist for ICH. Management of ICH is largely supportive, with strategies aimed at the limitation of further brain injury and the prevention of associated complications, which add further detrimental effects to an already lethal disease and jeopardise clinical outcomes. Complications of ICH include haematoma expansion, perihaematomal oedema with increased intracranial pressure, intraventricular extension of haemorrhage with hydrocephalus, seizures, venous thrombotic events, hyperglycaemia, increased blood pressure, fever, and infections. In view of the restricted number of therapeutic options for patients with ICH, improved surveillance is needed for the prevention of these complications, or, when this is not possible, early detection and optimum management, which could be effective in the reduction of adverse effects early in the course of stroke and in the improvement of prognosis. Further studies are needed to enhance the evidence-based recommendations for the management of this important clinical problem. Copyright © 2012 Elsevier Ltd. All rights reserved.
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            Electrical impedance tomography (EIT): a review.

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            Electrical impedance tomography (EIT) has been the subject of quite intensive research for about 20 years but has yet to become established as a routine tool in healthcare. None the less the volume of published research work in this area is still rising. This review takes a broad look at what has been achieved and attempts to give the reader sufficient information to form an opinion as to the likely future for this interesting area of research.
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              Cell death mechanisms following traumatic brain injury.

              Neuronal and glial cell death and traumatic axonal injury contribute to the overall pathology of traumatic brain injury (TBI) in both humans and animals. In both head-injured humans and following experimental brain injury, dying neural cells exhibit either an apoptotic or a necrotic morphology. Apoptotic and necrotic neurons have been identified within contusions in the acute post-traumatic period, and in regions remote from the site of impact in the days and weeks after trauma, while degenerating oligodendrocytes and astrocytes have been observed within injured white matter tracts. We review and compare the regional and temporal patterns of apoptotic and necrotic cell death following TBI and the possible mechanisms underlying trauma-induced cell death. While excitatory amino acids, increases in intracellular calcium and free radicals can all cause cells to undergo apoptosis, in vitro studies have determined that neural cells can undergo apoptosis via many other pathways. It is generally accepted that a shift in the balance between pro- and anti-apoptotic protein factors towards the expression of proteins that promote death may be one mechanism underlying apoptotic cell death. The effect of TBI on cellular expression of survival promoting-proteins such as Bcl-2, Bcl-xL, and extracellular signal-regulated kinases, and death-inducing proteins such as Bax, c-Jun N-terminal kinase, tumor-suppressor gene, p53, and the calpain and caspase families of proteases are reviewed. In light of pharmacologic strategies that have been devised to reduce the extent of apoptotic cell death in animal models of TBI, our review also considers whether apoptosis may serve a protective role in the injured brain. Together, these observations suggest that cell death mechanisms may be representative of a continuum between apoptotic and necrotic pathways.
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                Author and article information

                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group
                2045-2322
                29 November 2016
                2016
                : 6
                : 37620
                Affiliations
                [1 ]School of ITEE, The University of Queensland , St Lucia, 4072, Brisbane, Australia
                Author notes
                Article
                srep37620
                10.1038/srep37620
                5126641
                27897197
                04875bc1-2c24-4af2-a5c2-472fd9c27c0d
                Copyright © 2016, The Author(s)

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                : 18 April 2016
                : 01 November 2016
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