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Books on the topic 'Muscle ageing'
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1
Blanchard, Christal. Calcineurin signaling in ageing skeletal muscle. Sudbury, Ont: Laurentian University, 2005.
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2
Skelton, Dawn. Exercise for healthy ageing: Exercise programmes proven in research to increase muscle strength. 2nd ed. London: Research into Ageing, 1998.
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3
Kainulainen, Heikki. Effects of chronic exercise and ageing on regional energy metabolism in heart muscle. Jyväskylä: University of Jyväskylä, 1990.
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4
Lintz, Yannick. Le Musée des beaux-arts, Agen. Paris: Fondation BNP Paribas, 2000.
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5
Yannick, Lintz, Nivière Marie-Dominique, Amandry Michel, and Aboussouan Camille, eds. Visions d'Orient: Des cités mésopotamiennes à la Jérusalem des croisés : la donation Camille Aboussouan. Paris: Réunion des musées nationaux, 2002.
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6
Echenberg, Margo. The Fame of Sor Juana Inés de la Cruz. Nieuwe Prinsengracht 89 1018 VR Amsterdam Nederland: Amsterdam University Press, 2023. http://dx.doi.org/10.5117/9789463727044.
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The Fame of Sor Juana Inés de la Cruz traces the meteoric trajectory of the Mexican Tenth Muse’s renown and studies how her worldly celebrity was altered posthumously by elegists in her Fama y obras póstumas [Fame and Posthumous Works] of 1700. In this study of a polyphonic, transatlantic volume, the didactic framework of early modern fame is pushed to its limits as panegyrists inscribe the nun into an evolving world-view that could trade in the fictions of the saintly exemplar, the Tenth Muse or a New World treasure, but could not preserve a woman’s renown on the grounds of authorship. Only by making her legible could she vie for the promise of posthumous fame. In flushing out the machinations of Sor Juana’s role as agent of her own celebrity as well as the negotiations of her contemporaries, this book opens new lines of inquiry in the study of early modern fame and print culture and the role of writers, panegyrists and editors as cultural agents in the transatlantic literary relationship between Mexico and Spain.
7
1967-, Sandell Richard, Dodd Jocelyn, and Garland-Thomson Rosemarie, eds. Re-presenting disability: Activism and agency in the museum. New York: Routledge, 2010.
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8
1967-, Sandell Richard, Dodd Jocelyn, and Garland-Thompson Rosemarie, eds. Re-presenting disability: Activism and agency in the museum. New York: Routledge, 2010.
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9
Dinser, Robert, and Ulf Müller-Ladner. Skeletal muscle physiology and damage. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0055.
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This chapter summarizes muscle structure and physiology, the genesis and adaptions of muscle throughout life, and clinical assessment of muscle disease. The anatomical and molecular structure of muscle tissue is described, as well as the basic function of the neuromuscular junction, the energy metabolism of muscle tissue, and the mechanisms of fatigue. Key elements of embryological myogenesis, the adaptions of muscle to exercise and damage, and physiological ageing are depicted. A summary of the clinical analysis of muscle function including laboratory, electrophysiological, and imaging testing is provided.
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Dinser, Robert, and Ulf Müller-Ladner. Skeletal muscle physiology and damage. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0055_update_001.
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This chapter summarizes muscle structure and physiology, the genesis and adaptions of muscle throughout life, and clinical assessment of muscle disease. The anatomical and molecular structure of muscle tissue is described, as well as the basic function of the neuromuscular junction, the energy metabolism of muscle tissue, and the mechanisms of fatigue. Key elements of embryological myogenesis, the adaptions of muscle to exercise and damage, and physiological ageing are depicted. A summary of the clinical analysis of muscle function including laboratory, electrophysiological, and imaging testing is provided.
11
Machado, Pedro M. Inclusion body myositis. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0011.
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Sporadic inclusion body myositis (IBM) is an acquired muscle disorder associated with ageing, for which there is no effective treatment. It is characterized by a typical early clinical phenotype with (often asymmetric) weakness of the knee extensors and finger flexors, potential involvement of pharyngeal and upper-oesophageal muscles (which may contribute to malnutrition and aspiration), and progressive and slow deterioration, which may lead to severe disability and loss of quality of life. Muscle biopsy shows chronic myopathic features, lymphocytic infiltration with invasion of non-necrotic fibres, rimmed vacuoles, mitochondrial changes, and pathological accumulation of proteins in the muscle tissue. It remains uncertain whether IBM is primarily an immune-mediated inflammatory myopathy or a degenerative myopathy with an associated inflammatory component. This chapter will describe the clinical features, natural history, investigations, current pathogenic concepts, outcome measures, and therapeutic approaches in IBM. Despite recent clues, in many respects IBM remains an unsolved mystery.
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Dodds, Chris, Chandra M. Kumar, and Frédérique Servin. Anaesthetic pharmacology in the elderly. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198735571.003.0003.
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The importance of the changes and variability in pharmacology with ageing and the risks these pose in the elderly are emphasized. Detailed descriptions are given of the pharmacokinetic aspects of distribution, initial volume of distribution, and plasma binding; elimination affected by hepatic and renal clearance changes; and effect site variability. The pharmacodynamics changes are then reviewed. Specific anaesthetic agents are then described, covering the induction agents thiopentone, propofol, etomidate, ketamine, and midazolam. The volatile anaesthetics sevoflurane and desflurane, and nitrous oxide are discussed. The opioid analgesics fentanyl, alfentanil, sufentanil, and remifentanil are described followed by the opiate morphine. The much slower onset and offset of muscle relaxants in the elderly is explained, and the differences between steroid and benzylisoquinolinium compounds are described. Finally, the reversal agents, including sugammadex, are reviewed.
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Pollard, Brian J. Muscle relaxants in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0047.
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The place of neuromuscular blocking agents in the intensive care unit (ICU) has changed markedly over the last 20 years. Originally regarded as a mainstay of the process of ‘sedation’, they are now only used for specific indications. The principal disadvantage is probably the difficulty in neurological assessment when a muscle relaxant is used coupled with the increased risk of awareness, because inadequate sedation will be masked. Of the available agents, the intermediate acting ones are the most popular. The degree of relaxation can be readily controlled and they have few side effects. In the presence of renal and/or hepatic disease atracurium or cisatracurium are preferred. Succinylcholine is only used for securing the airway due to its very rapid onset of action. Rocuronium given in a higher dose also possesses a rapid onset in situations when succinylcholine might be contraindicated. When using a muscle relaxant, its effect should always be monitored with a simple train of four pattern of stimulation from a hand-held nerve stimulator. This will ensure that an adequate and not excessive block is secured. If a more rapid reversal is required then a dose of neostigmine with glycopyrrolate may be used. Alternatively, if rocuronium is the relaxant in use then the new agent sugammadex is effective.
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Lahouti, Arash H., and Lisa Christopher-Stine. Toxic myopathies. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0009.
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Toxic myopathy symptoms range from myalgia and muscle cramps to severe weakness, bearing similarities to a number of other muscle conditions. Thus, when evaluating patients with muscle symptoms, an iatrogenic muscle problem should always be considered, to be able to distinguish a toxic from any other myopathy early on, preventing further muscle damage and to potentially reverse muscle injury by withdrawal of the toxic agent. Various commonly prescribed medications, as well as illicit drugs, may cause muscle damage. These substances may cause muscle injury through direct myotoxic effects, or indirectly through various mechanisms, such as electrolyte abnormalities and triggering, or disinhibiting the immune system response.
15
Guire, Michelle Mc. The influence of streptozotcin diabetes and the hypoglycaemic agent metformin on rat skeletal muscles. 1997.
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16
Heine, Christopher L. Malignant Hyperthermia. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0025.
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In this chapter we discuss the pathophysiology of malignant hyperthermia, identify those who are known to be susceptible to MH, delineate how best to prepare the operating for those patients, and provide step by step treatment recommendations for patients that develop MH. Malignant hyperthermia (MH) is a pharmacogenetic disease. When susceptible individuals are exposed to a triggering agent, a hypermetabolic response develops. Succinylcholine and halogenated, inhaled anesthetics are triggers of MH. The MH reaction is initiated by a rapid influx of calcium ions into the myoplasm that triggers uncontrolled muscle contraction. Prompt recognition and treatment of the reaction is critical to a successful outcome.
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Flisser, Ana, Philip S. Craig, and Akira Ito. Cysticercosis and taeniosis: Taenia solium, Taenia saginata and Taenia asiatica. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0058.
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The pork and beef tapeworms, Taenia solium and Taenia saginata respectively, are taeniid cestodes and major food-borne or meat-borne zoonoses. Human tapeworms and swine cysticerci have been known since Egyptian and Greek cultures. Nevertheless their association as part of the life cycle of the same parasite was only demonstrated during the nineteenth century. Kuchenmeister fed convicts with cysticerci excised from pork meat and found adult tapeworms in the intestine after autopsy, while van Beneden fed T. solium eggs to pigs and found numerous cysticerci in muscles after slaughter (Grove, 1990).T. solium is the only causative agent of neurocysticercosis in humans and is, therefore, the more important of these species in public health. This chapter describes classical aspects of the morphology of the parasites as well as clinical aspects of the diseases they cause. Most importantly, detailed explanations of taxonomic aspects, specially related to the newly recognized Taenia asiatica are given. Furthermore, the epidemiology and transmission dynamics of the parasites, as well as intervention measures such as health education, mass drug treatment and vaccination, are described in detail. The chapter concludes with considerations on the surveillance and a discussion on prospects for the control of these cestode zoonoses.
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Levtchenko, Elena N., and Mirian C. Janssen. Cystinosis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0339_update_001.
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Cystinosis is a rare autosomal recessive disease caused by mutations in the lysosomal cystine transporter cystinosin encoded by the CTNS gene (17p.13.2). Cystinosis is characterized by lysosomal cystine accumulation throughout the body with renal Fanconi syndrome being the most common presenting symptom of a multisystem disorder. It must be distinguished from cystinuria in which formation of cystine stones is the core problem. When left untreated, kidney dysfunction gradually progresses towards end-stage renal failure during the first 10 years of life. The advent of renal replacement therapy allowed cystinosis patients to survive into adulthood, but revealed numerous extrarenal manifestations of the disease, affecting eyes, endocrine organs, gastrointestinal tract, muscles, and central and peripheral nervous systems. The disease mechanism of cystinosis is not fully understood. The administration of the cystine-depleting agent cysteamine slows down renal and extrarenal organ damage, pointing to the pivotal role of cystine accumulation in the disease pathogenesis. Treatment with cysteamine should be initiated as early as possible and continued lifelong, and also after kidney transplantation for protecting extrarenal organs. Cysteamine eye drops are an indispensable part of the treatment of corneal cystine accumulation. Life expectancy of cystinosis patients has substantially improved and is now above 50 years.
19
Dasgupta, Bhaskar. Polymyalgia rheumatica. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0134.
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This chapter reviews advances in pathogenesis; European League Against Rheumatism/American College of Rheumatology (EULAR/ACR) classification criteria with clinical, laboratory, and ultrasound criteria for classification as polymyalgia rheumatica (PMR); the heterogeneity and overlap between PMR, inflammatory arthritis, and large-vessel vasculitis as illustrated by representative cases; recent guidelines on early and correct recognition, investigations, and management of PMR; the scope of disease-modifying agents; socio-economic impact, outcomes, and patient experience in PMR. It also discusses areas for future research including clinical trials with biological agents and newer steroid formulations, standardized outcome assessments, and the search for better biomarkers in PMR. PMR is one of the common inflammatory rheumatic diseases of older people and represents a frequent indication for long-term glucocorticoid (GC) therapy. It is characterized by abrupt-onset pain and stiffness of the shoulder and pelvic girdle muscles. Its management is subject to wide variations of clinical practice and it is managed in primary or secondary care by general practitioners (GPs), rheumatologists, and non-rheumatologists. The evaluation of PMR can be challenging, as many clinical and laboratory features may also be present in other conditions, including other rheumatological diseases, infection, and neoplasia. PMR is usually diagnosed in the primary care setting, but standard clinical investigations and referral pathways for suspected PMR are unclear. The response to standardized therapy is heterogeneous, and a significant proportion of patients do not respond completely. There is also an overlap with inflammatory arthritis and large-vessel vasculitis for which adjuvant disease-modifying medications are often used. Prolonged corticosteroid therapy is associated with a variety of side effects, especially when high-dose glucocorticoid therapy is employed. Giant cell arteritis (GCA) is also often linked to PMR. It is a vasculitis of large- and medium-sized vessels causing critical ischaemia. GCA is a medical emergency because of the high incidence of neuro-ophthalmic complications. Both conditions are associated with a systemic inflammatory response and constitutional symptoms. The pathogenesis is unclear. The initiating step may be the recognition of an infectious agent by aberrantly activated dendritic cells. The key cell types involved are CD4+ T cells and macrophages giving rise to key cytokines such as interferon-γ (implicated in granuloma formation), PDGF (intimal hyperplasia), and interleukin (IL)-6 (key to the systemic response). The pathogenesis of PMR may be similar to that of GCA, although PMR exhibits less clinical vascular involvement. The mainstay of therapy is corticosteroids, and disease-modifying therapy is currently indicated in relapsing disease.
20
Shaw, Pamela, and David Hilton-Jones. The lower cranial nerves and dysphagia. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0429.
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Disorders affecting the lower cranial nerves – V (trigeminal), VII (facial), IX (glossopharyngeal), X (vagus), XI (accessory) and XII (hypoglossal) – are discussed in the first part of this chapter. The clinical neuroanatomy of each nerve is described in detail, as are disorders – often in the form of lesions – for each nerve.Trigeminal nerve function may be affected by supranuclear, nuclear, or peripheral lesions. Because of the wide anatomical distribution of the components of the trigeminal nerve, complete interruption of both the motor and sensory parts is rarely observed in practice. However, partial involvement of the trigeminal nerve, particularly the sensory component, is relatively common, the main symptoms being numbness and pain. Reactivation of herpes zoster in the trigeminal nerve (shingles) can cause pain and a rash. Trigeminal neuralgia and sensory neuropathy are also discussed.Other disorders of the lower cranial nerves include Bell’s palsy, hemifacial spasm and glossopharyngeal neuralgia. Cavernous sinus, Tolosa–Hunt syndrome, jugular foramen syndrome and polyneuritis cranialis are caused by the involvement of more than one lower cranial nerve.Difficulty in swallowing, or dysphagia, is a common neurological problem and the most important consequences include aspiration and malnutrition (Wiles 1991). The process of swallowing is a complex neuromuscular activity, which allows the safe transport of material from the mouth to the stomach for digestion, without compromising the airway. It involves the synergistic action of at least 32 pairs of muscles and depends on the integrity of sensory and motor pathways of several cranial nerves; V, VII, IX, X, and XII. In neurological practice dysphagia is most often seen in association with other, obvious, neurological problems. Apart from in oculopharyngeal muscular dystrophy, it is relatively rare as a sole presenting symptom although occasionally this is seen in motor neurone disease, myasthenia gravis, and inclusion body myositis. Conversely, in general medical practice, there are many mechanical or structural disorders which may have dysphagia as the presenting feature. In some of the disorders, notably motor neurone disease, both upper and lower motor neurone dysfunction may contribute to the dysphagia. Once dysphagia has been identified as a real or potential problem, the patient should undergo expert evaluation by a clinician and a speech therapist, prior to any attempt at feeding. Videofluoroscopy may be required. If there is any doubt it is best to achieve adequate nutrition through the use of a fine-bore nasogastric tube and to periodically reassess swallowing. Anticholinergic drugs may be helpful to reduce problems with excess saliva and drooling that occur in patients with neurological dysphagia, and a portable suction apparatus may be helpful. Difficulty in clearing secretions from the throat may be helped by the administration of a mucolytic agent such as carbocisteine or provision of a cough assist device.
21
Sandell, Richard, Rosemarie Garland-Thomson, and Jocelyn Dodd. Re-Presenting Disability: Activism and Agency in the Museum. Taylor & Francis Group, 2013.
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22
Sandell, Richard, Rosemarie Garland-Thomson, and Jocelyn Dodd. Re-Presenting Disability: Activism and Agency in the Museum. Taylor & Francis Group, 2013.
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