4,632 research outputs found

    Mitochondria as Crucial Players in Demyelinated Axons: Lessons from Neuropathology and Experimental Demyelination

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    Mitochondria are the most efficient producers of energy in the form of ATP. Energy demands of axons, placed at relatively great distances from the neuronal cell body, are met by mitochondria, which when functionally compromised, produce reactive oxygen species (ROS) in excess. Axons are made metabolically efficient by myelination, which enables saltatory conduction. The importance of mitochondria for maintaining the structural integrity of myelinated axons is illustrated by neuroaxonal degeneration in primary mitochondrial disorders. When demyelinated, the compartmentalisation of ion channels along axons is disrupted. The redistribution of electrogenic machinery is thought to increase the energy demand of demyelinated axons. We review related studies that focus on mitochondria within unmyelinated, demyelinated and dysmyelinated axons in the central nervous system. Based on neuropathological observations we propose the increase in mitochondrial presence within demyelinated axons as an adaptive process to the increased energy need. An increased presence of mitochondria would also increase the capacity to produce deleterious agents such as ROS when functionally compromised. Given the lack of direct evidence of a beneficial or harmful effect of mitochondrial changes, the precise role of increased mitochondrial presence within axons due to demyelination needs to be further explored in experimental demyelination in-vivo and in-vitro

    Application of Additive Manufacturing to the Digital Restoration of Archaeological Artifacts

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    AbstractThis paper reports a substantial body of work that has been done in this area, which has been used to determine how Additive Manufacturing (AM) and subsequent processes should be optimally applied, and introduces a series of process maps that have been generated to guide future practical work with a combination of questionnaires and expert interviews for validating the process maps. The outputs from the research should prove to be valuable to anyone working in this field. The main contribution to knowledge is the characterisation of archaeological artefacts and the resultant process maps derived from this characterization

    Circuit Theory and Design

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    Contains research objectives and reports on one research projects.U. S. Air Force under Air Force Contract AF19(604)-5200U. S. NavyU. S. ArmyLincoln Laboratory, Purchase Order DDL B-0030

    Pain assessment and pain treatment for community-dwelling people with dementia: A systematic review and narrative synthesis.

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    OBJECTIVES: To describe the current literature on pain assessment and pain treatment for community-dwelling people with dementia. METHOD: A comprehensive systematic search of the literature with narrative synthesis was conducted. Eight major bibliographic databases were searched in October 2018. Titles, abstracts, and full-text articles were sequentially screened. Standardised data extraction and quality appraisal exercises were conducted. RESULTS: 32 studies were included in the review, 11 reporting findings on pain assessment tools or methods, and 27 reporting findings on treatments for pain. In regard to pain assessment, a large proportion of people with moderate to severe dementia were unable to complete a self-report pain instrument. Pain was more commonly reported by informal caregivers than the person with dementia themselves. Limited evidence was available for pain focused behavioural observation assessment. In regard to pain treatment, paracetamol use was more common in community-dwelling people with dementia compared to people without dementia. However, non-steroidal anti-inflammatory drugs (NSAIDs) were used less. For stronger analgesics, community-dwelling people with dementia were more likely to receive strong opioids (e.g. fentanyl) than people without dementia. CONCLUSION: This review identifies a dearth of high quality studies exploring pain assessment and/or treatment for community-dwelling people with dementia, not least into non-pharmacological interventions. The consequences of this lack of evidence, given the current and projected prevalence of the disease, are very serious and require urgent redress. In the meantime, clinicians should adopt a patient and caregiver centred, multi-dimensional, longitudinal approach to pain assessment and pain treatment for this population

    Cinnamon Shows Antidiabetic Properties that Are Species-Specific : Effects on Enzyme Activity Inhibition and Starch Digestion

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    The study was funded by the Rural and Environment Science and Analytical Services Division of the Scottish government (RESAS). The authors are grateful to Phyllis Nicol for assisting with AGE measurements.Peer reviewedPublisher PD

    No excess of mitochondrial DNA deletions within muscle in progressive multiple sclerosis

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    BACKGROUND: Mitochondrial dysfunction is an established feature of multiple sclerosis (MS). We recently described high levels of mitochondrial DNA (mtDNA) deletions within respiratory enzyme-deficient (lacking mitochondrial respiratory chain complex IV with intact complex II) neurons and choroid plexus epithelial cells in progressive MS. OBJECTIVES: The objective of this paper is to determine whether respiratory enzyme deficiency and mtDNA deletions in MS were in excess of age-related changes within muscle, which, like neurons, are post-mitotic cells that frequently harbour mtDNA deletions with ageing and in disease. METHODS: In progressive MS cases (n=17), known to harbour an excess of mtDNA deletions in the central nervous system (CNS), and controls (n=15), we studied muscle (paraspinal) and explored mitochondria in single fibres. Histochemistry, immunohistochemistry, laser microdissection, real-time polymerase chain reaction (PCR), long-range PCR and sequencing were used to resolve the single muscle fibres. RESULTS: The percentage of respiratory enzyme-deficient muscle fibres, mtDNA deletion level and percentage of muscle fibres harbouring high levels of mtDNA deletions were not significantly different in MS compared with controls. CONCLUSION: Our findings do not provide support to the existence of a diffuse mitochondrial abnormality involving multiple systems in MS. Understanding the cause(s) of the CNS mitochondrial dysfunction in progressive MS remains a research priority
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