23 research outputs found

    Neuroprotection with the N-methyl-D-aspartate antagonist dizocilpine (MK-801) in a model of focal ischaemia

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    Ischaemic brain damage, due to cerebrovascular disease ("stroke"), head injury, cardiac arrest, surgery (cardiopulmonary bypass and intracranial) and perinatal hypoxia, is a major cause of death and disability in the western world. Stroke alone is the third most common cause of death after cancer and heart disease, accounting for some 10% of all deaths, approximately 60,000 per year in England and Wales. Recently there has been rapidly growing evidence supporting the "excitotoxic" theory of neuronal damage in ischaemia, in which excitatory amino acid neurotransmitters are implicated as agents of damage to ischaemic brain. Excitatory amino acid antagonists, in particular N-methyl-D-aspartate (NMDA) antagonists, have proved to be dramatically effective in the protection of brain parenchyma in experimental models of ischaemia, especially focal ischaemia. The role of excitatory amino acid neurotransm itters in ischaemia and the experimental evidence for amelioration of ischaemic brain damage by NMDA antagonists, is reviewed. A model of focal ischaemia in the rat is described, which can be used for assessing drugs that might be useful clinically. A method of volumetric analysis of infarct size using conventional histopathology is compared to a much cheaper and faster m ethod using the m itochondrial redox stain, 2,3,5,triphenyltetrazolium chloride (TTC). The later method can be used for the rapid screening of compounds, but it has limitations which are fully explored. The neuroprotective effects of the NMDA antagonist, dizocilpine (MK-801) in acute and chronic ischaemia are compared and the chronic model is used to establish a "dose response" and "therapeutic window" for dizocilpine. Hypertension is a major risk factor in stroke and the neuroprotective effects of dizocilpine are examined in both normotensive and spontaneously hypertensive strains of rat, with pure cortical and combined cortical and striatal lesions. Finally, release of neuron-specific enolase into the CSF is correlated with infarct size in dizocilpine treated and control animals with a view to the possible clinical use of NSE in the quantification of ischaemic damage

    Modelling magnetic diffusion and decadal geomagnetic secular variation

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    Changes in the magnetic field generated within Earth's core that occur over years to centuries are known as geomagnetic secular variation (SV). These temporal variations arise from motions of the electrically conducting outer core fluid, and magnetic diffusion. Diffusive field changes are often considered much slower than those associated with fluid flow. For yearly to decadal SV, diffusion is therefore neglected in the widely adopted frozen-flux approximation. However, several studies have stressed the incompatibility of frozen flux with the SV observed over the 20th century. In particular, the approximation conflicts with the emergence of reversed-flux patches (RFPs) on the core-mantle boundary (CMB), which are regions where the sign of radial magnetic field differs from the otherwise prevalent dipole field aligned with Earth's rotation axis (i.e. the axial dipole field). In this thesis, we first introduce a method to characterise RFPs and their evolution. Subsequently, we show how these features have proliferated, strengthened, and migrated towards the geographic poles, matching the observed weakening of the axial dipole. We introduce a formalism allowing the inversion of the observed SV for an initial magnetic field throughout the core, assuming purely diffusive SV. With this method we demonstrate that pure diffusion is consistent with the SV over several decades, and can reproduce fundamental SV characteristics such as westward drift, recent North Magnetic Pole acceleration, and reversed-flux emergence. We also use our inverse formalism to augment frozen-flux models for core fluid motion by including magnetic diffusion. This hybrid scheme is shown to more accurately predict yearly SV than steady core flow, in particular that of South Atlantic RFPs. Finally, we use this hybrid forecasting method to compute a candidate model for the 2020.0 International Geomagnetic Reference Field. Our predictions also show how future axial dipole decay is no longer due to poleward migration of RFPs

    Contralateral responses to an inflammatory stimulus in man

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    Scientific Information on Gulf of Mannar - A Bibliography

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    Gulf of Mannar in the southeast coast of India extends from Rameswaram Island in the north to Kanyakumari in the south. It has a chain of 21 islands stretching from Mandapam to Tuticorin to a distance of 140 km along the coast. Each one of the islands is located anywhere between 2 and 10 km from the mainland. The Gulf of Mannar Biosphere Reserve was set up on 18th February 1989 jointly by the Government of India and the state of Tamilnadu. The government of Tamilnadu in G.O. M.S. No 962 dated 10th September 1986 notified under section 35(1) of the Wildlife (Protection) Act 1972 the intention to declare the 21 islands as Marine National Park for the purpose of protecting marine wildlife and its environment including depths of 3.5 fathoms on the bay side to 5 fathoms on the seaward side. The compilation of all available scientific literature in the form of an annotated bibliography of the Gulf of Mannar biosphere reserve has brought to light the existence of nearly 3,000 publications up to date. This covers the literature published from as early as 1864 to the current year. A large number of publications in the first half of the 20th century have brought out information on the variety of fauna and flora found in the Gulf of Mannar, their biology and ecology. A lot of emphasis on the fish and fisheries research has been given only in the second half of the 20th century. Emphasis is being given on biochemical aspects of flora and fauna in the later part of the 20th century and at present

    Peripheral Neuropathy

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    Understanding the rapid changes in the evaluation and management of peripheral neuropathies, as well as the complexity of their mechanism, is a mandatory requirement for the practitioner to optimize patient's care. The objective of this book is to update health care professionals on recent advances in the pathogenesis, diagnosis and treatment of peripheral neuropathy. This work was written by a group of clinicians and scientists with large expertise in the field
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