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Books on the topic 'Mechanical activation'

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Published: 4 June 2021
Last updated: 22 February 2023

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1

Mechanical activation of minerals. Amsterdam: Elsevier, 1989.

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2

Ristić, Momčilo M. Mechanical activation of inorganic materials. Edited by Milošević Siniša Dj and Miljanić Petar. Belgrade: Serbian Academy of Science and Arts, 1998.

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3

Ristić, Momčilo M. Mechanical activation of inorganic materials. Edited by Milošević Siniša Dj and Miljanić Petar. Belgrade: Serbian Academy of Science and Arts, 1998.

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4

Mechanical activation of minerals by grinding: Pulverizing and morphology of particles. Chichester: Ellis Horwood, 1990.

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5

Dr, Juhász Z. Mechanical activation of minerals by grinding: Pulverizing and morphology of particles. Budapest: Akadémiai Kiadó, 1990.

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6

Sudhir, Gupta, Paul William E, and Fauci Anthony S. 1940-, eds. Mechanisms of lymphocyte activation and immune regulation. New York: Plenum Press, 1987.

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7

Sudhir, Gupta, Paul William E, and Fauci Anthony S, eds. Mechanisms of lymphocyte activation and immune regulation. New York: Plenum Press, 1987.

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8

International Conference on Mechanochemistry and Mechanical Activation (2nd 1997 Novosibirsk, Russia). INCOME-2, 2-nd International Conference on Mechanochemistry and Mechanical Activation: Novosibirsk, Russia, 12-16 August, 1997 : program and abstracts. [Novosibirsk?]: Institute of Solid State Chemistry, Siberian Branch, Russian Academy of Sciences, 1997.

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9

Boldyrev, V. V. Mechanochemistry and Mechanical Activation of Solids. Imperial College Press, 2006.

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10

Juhasz, Z. Mechanical activation of minerals by grinding: Pulverizing and morphology of particles. Akademiai Kiado, 1990.

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11

Fauci, Anthony S. Mechanisms of Lymphocyte Activation and Immune Regulation. Springer London, Limited, 2013.

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12

Fauci, Anthony S. Mechanisms of Lymphocyte Activation and Immune Regulation. Springer, 2012.

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13

H, Vandenburgh Herman, and United States. National Aeronautics and Space Administration., eds. Mechanical stimulation of skeletal muscle generates lipid-related second messengers by phospholipase activation. [Washington, DC?: National Aeronautics and Space Administration, 1991.

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14

Fauci, Anthony S. Mechanisms of Lymphocyte Activation and Immune Regulation (Advances in Experimental Medicine and Biology). Springer, 1987.

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15

The effects of lifting posture and muscular fatigue on erector spinae activation in normals and weight lifters. 1991.

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16

The effects of lifting posture and muscular fatigue on erector spinae activation in normals and weight lifters. 1991.

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17

The effects of lifting posture and muscular fatigue on erector spinae activation in normals and weight lifters. 1990.

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18

Dutto, Darren John. Leg spring model related to muscle activation, force, and kinematic patterns during endurance running to voluntary exhaustion. 1999.

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19

Ware, Lorraine B. Pathophysiology of acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0108.

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The acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure characterized by the acute onset of non-cardiogenic pulmonary oedema due to increased lung endothelial and alveolar epithelial permeability. Common predisposing clinical conditions include sepsis, pneumonia, severe traumatic injury, and aspiration of gastric contents. Environmental factors, such as alcohol abuse and cigarette smoke exposure may increase the risk of developing ARDS in those at risk. Pathologically, ARDS is characterized by diffuse alveolar damage with neutrophilic alveolitis, haemorrhage, hyaline membrane formation, and pulmonary oedema. A variety of cellular and molecular mechanisms contribute to the pathophysiology of ARDS, including exuberant inflammation, neutrophil recruitment and activation, oxidant injury, endothelial activation and injury, lung epithelial injury and/or necrosis, and activation of coagulation in the airspace. Mechanical ventilation can exacerbate lung inflammation and injury, particularly if delivered with high tidal volumes and/or pressures. Resolution of ARDS is complex and requires coordinated activation of multiple resolution pathways that include alveolar epithelial repair, clearance of pulmonary oedema through active ion transport, apoptosis, and clearance of intra-alveolar neutrophils, resolution of inflammation and fibrinolysis of fibrin-rich hyaline membranes. In some patients, activation of profibrotic pathways leads to significant lung fibrosis with resultant prolonged respiratory failure and failure of resolution.
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20

Henriksen, Niels Engholm, and Flemming Yssing Hansen. Unimolecular Reactions. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198805014.003.0007.

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This chapter considers unimolecular reactions; photo-induced reactions, that is, true unimolecular reactions; and reactions initiated by collisional activation, that is, apparent unimolecular reactions where it is assumed that the time scales for activation and subsequent reaction are well separated. Elements of classical and quantum dynamical descriptions are discussed, including Slater theory and the quantum mechanical description of photo-induced reactions. Statistical theories aiming at the calculation of micro-canonical as well as canonical rate constants are discussed, including a detailed discussion of RRKM theory. It concludes with a discussion of femtochemistry, that is, the observation and control of chemical dynamics using femtosecond pulses of electromagnetic radiation, focusing on the control of unimolecular reactions via the interaction with coherent light; that is, laser control.
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21

Biewener, Andrew A., and Shelia N. Patek, eds. Muscles and Skeletons. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198743156.003.0002.

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Animal locomotion depends on the organization, physiology and biomechanical properties of muscles and skeletons. Musculoskeletal systems encompass the mechanical interactions of muscles and skeletal elements that ultimately transmit force for movement and support. Muscles not only perform work by contracting and shortening to generate force, they can also operate as brakes to slow the whole body or a single appendage. Muscles can also function as struts (rod-like) to maintain the position of a joint and facilitate elastic energy storage and recovery. Skeletal muscles share a basic organization and all rely on the same protein machinery for generating force and movement. Variation in muscle function, therefore, depends on the underlying mechanical and energetic components, enzymatic properties, and activation by the nervous system. Muscles require either an internal, external or hydrostatic skeletal system to transmit force for movement and support.
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22

Schaible, Hans-Georg, and Rainer H. Straub. Pain neurophysiology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0059.

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Physiological pain is evoked by intense (noxious) stimuli acting on healthy tissue functioning as a warning signal to avoid damage of the tissue. In contrast, pathophysiological pain is present in the course of disease, and it is often elicited by low-intensity stimulation or occurs even as resting pain. Causes of pathophysiological pain are either inflammation or injury causing pathophysiological nociceptive pain or damage to nerve cells evoking neuropathic pain. The major peripheral neuronal mechanism of pathophysiological nociceptive pain is the sensitization of peripheral nociceptors for mechanical, thermal and chemical stimuli; the major peripheral mechanism of neuropathic pain is the generation of ectopic discharges in injured nerve fibres. These phenomena are created by changes of ion channels in the neurons, e.g. by the influence of inflammatory mediators or growth factors. Both peripheral sensitization and ectopic discharges can evoke the development of hyperexcitability of central nociceptive pathways, called central sensitization, which amplifies the nociceptive processing. Central sensitization is caused by changes of the synaptic processing, in which glial cell activation also plays an important role. Endogenous inhibitory neuronal systems may reduce pain but some types of pain are characterized by the loss of inhibitory neural function. In addition to their role in pain generation, nociceptive afferents and the spinal cord can further enhance the inflammatory process by the release of neuropeptides into the innervated tissue and by activation of sympathetic efferent fibres. However, in inflamed tissue the innervation is remodelled by repellent factors, in particular with a loss of sympathetic nerve fibres.
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23

L, Purich Daniel, ed. Enzyme kinetics and mechanism. San Diego: Academic Press, 2002.

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24

Leys, Didier, Charlotte Cordonnier, and Valeria Caso. Stroke. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0067_update_002.

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Stroke is a major public health issue. Many are treatable in the acute stage, provided patients are admitted soon enough. The overall incidence of stroke in Western countries is approximately 2400 per year per million inhabitants, and 80% are due to cerebral ischaemia. The prevalence is approximately 12 000 per million inhabitants. Stroke is associated with increased long-term mortality, handicap, cognitive and behavioural impairments, recurrence, and an increased risk of other types of vascular events. It is of major interest to take the heterogeneity of stroke into account, because of differences in the acute management, secondary prevention, and outcomes, according to the subtype and cause of stroke. In all types of stroke, early epileptic seizures, delirium, increased intracranial pressure, and non-specific complications are frequent. In ischaemic strokes, specific complications, such as malignant infarcts, spontaneous haemorrhagic transformation, early recurrence, and a new ischaemic event in another vascular territory, are frequent. In haemorrhagic strokes, the major complication is the subsequent increased volume of bleeding. There is strong evidence that stroke patients should be treated in dedicated stroke units; each time 24 patients are treated in a stroke unit, instead of a conventional ward, one death and one dependence are prevented. This effect does not depend on age, severity, and the stroke subtype. For this reason, stroke unit care is the cornerstone of the treatment of stroke, aiming at the detection and management of life-threatening emergencies, stabilization of most physiological parameters, and prevention of early complications. In ischaemic strokes, besides this general management, specific therapies include intravenous recombinant tissue plasminogen activator, given as soon as possible and before 4.5 hours, mechanical thrombectomy in case of proximal occlusion (middle cerebral artery, intracranial internal carotid artery, basilar artery), on top of thrombolysis in the absence of contraindication or alone otherwise, aspirin 300 mg, immediately or after 24 hours in case of thrombolysis, and, in a few patients, decompressive surgery. In intracerebral haemorrhages, blood pressure lowering and haemostatic therapy, when needed, are the two targets, while surgery does not seem effective to reduce death and disability.
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