Books: 'Cascade disruption of generation'

1

Yamamoto, Atsumasa. Three-dimensional flows and loss generation mechanisms in a linear turbine rotor cascade at various incidence conditions. National Aerospace Laboratory, 1988.

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2

Black, Gerald L. Geothermal electrical power generation potential of Newberry Volcano and the Oregon Cascade Range. State of Oregon, Dept. of Geology and Mineral Industries, 1994.

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3

Grove, Darren V. Experimental and numerical investigation of second-generation, controlled-diffusion, compressor blades in cascade. Naval Postgraduate School, 1997.

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4

Aippersbach, Elke Daniela. Targeted disruption of the Grb4 and Nck loci and generation of homozygous null NCK mice. National Library of Canada, 1998.

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5

Esrada, Francisco J. Moncayo. Generation of wet steam of prescribed droplet size for admission to a cascade of blades. University of Birmingham, 1992.

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6

Parlato, Marianna, and Jean-Marc Cavaillon. Innate immunity and the inflammatory cascade. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0299.

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Inflammation results from a complex interaction between a large number of mediators able to induce each other and to favour the generation of other inflammatory molecules (e.g. free radicals, lipid mediators, and proteases). The perpetuation of inflammation by these cascades of mediators is favoured by their ability to induce coagulation, leukocyte recruitment, and cell and tissue alteration (apoptosis, necrosis, and barrier disruption). Other cascades of mediators occur to generate anti-inflammatory mediators favouring the healing process. A neuroendocrine loop and neuromediators from central and peripheral nervous system are also involved in the process, allowing a return to homeostasis.

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7

Investigation of Flow Over Second Generation Controlled-Diffusion Bladesin a Linear Cascade. Storming Media, 1999.

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8

Sollohub, Darius. Millennials in Architecture: Generations, Disruption, and the Legacy of a Profession. University of Texas Press, 2019.

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9

Millennials in Architecture: Generations, Disruption, and the Legacy of a Profession. University of Texas Press, 2019.

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10

Experimental and Numerical Investigation of Second-Generation, Controlled-Diffusion, Compressor Blades in Cascade. Storming Media, 1997.

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11

Examination of Flow Around Second-Generation Controlled Diffusion Compressor Blades in Cascade at Stall. Storming Media, 2004.

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12

Three-Component LDV Measurements of Corner Vortices over Second- Generation, Controlled-Diffusion, Compressor Blades in Cascade. Storming Media, 2001.

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13

Experimental Investigation of Vortex Shedding in Flow Over Second- Generation, Controlled-Diffusion, Compressor Blades in Cascade. Storming Media, 2002.

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14

Keightley, Emily, and Michael Pickering. The Mnemonic Imagination and Second-Generation Migrant Experience. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190468712.003.0008.

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Drawing on our concept of the mnemonic imagination, this chapter shows how the past is reactivated and pieced together into a relatively coherent narrative in the interests of identity and the effective management of change. In forming the synthetic hub of remembering and imagining, the mnemonic imagination is mobilized in bringing past, present, and future into meaningful correspondence. This chapter illustrates how this happens via an ethnographic case study involving Kia Kapoor, a second-generation Indian woman in her early 30s living in England, who uses her work as a professional photographer to help her negotiate her own difficult past as someone caught between two cultures. The case demonstrates mnemonic imagining at work in a particular cross-generational and cross-cultural context, taking into account how it can be thwarted by various obstacles and how, through considerable resistance and struggle, it can help overcome the consequences of radical sociocultural disruption.

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15

Mahta, Ali, and Peter B. Crino. Focal Cortical Dysplasias. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0039.

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Focal cortical dysplasias (FCDs) are common malformations of cerebral cortical development that are highly associated with medically intractable epilepsy. FCDs have been classified according to neuropathological subtypes (type Ia, Ib, IIA, IIb, and III) based on the severity of cytoarchitectural disruption, and the presence of unique cell types (e.g., balloon cells). Most FCDs can be detected by neuroimaging studies and will require respective epilepsy surgery to cure refractory seizures. The pathogenesis of FCDs remains to be defined, although current belief is that these lesions result from sporadic somatic mutations occurring in brain development. A link to the mammalian target of rapamycin cascade has been defined for some FCD subtypes.

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16

Dietrich, W. Dalton. Physiologic Modulators of Neural Injury After Brain and Spinal Cord Injury. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0001.

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Brain and spinal cord injury are leading causes of death and long-term disability, producing diverse burdens for the affected individuals, their families, and society. Such injuries, including traumatic brain injury, stroke, subarachnoid hemorrhage, and spinal cord injury, have common patterns of neuronal cell vulnerability that are associated with a complex cascade of pathologic processes that trigger the propagation of tissue damage beyond the acute injury. Secondary injury mechanisms, including oxidative stress, edema formation, changes in cerebral blood flow and vessel reactivity, metabolic and blood–brain barrier disruption, and neuroinflammation, are therefore important therapeutic targets. Several key physiological parameters require monitoring and intensive management during various phases of treatment to ameliorate secondary injury mechanisms and potentially protect against further neuronal injury. This chapter reviews the core physiological targets in the management of brain and spinal cord injury and relates them to secondary injury mechanisms and outcomes.

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17

Olmeda, José A., and César Colino. Leadership Capital in a Protracted Crisis. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198783848.003.0011.

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The last Spanish prime ministers, Zapatero and Rajoy, have had to deal with the effects of the 2007 economic crisis. The Leadership Capital Index is used to analyze their respective leaderships and shows how both leaders used, gained, or lost capital while seeking to deal with the severe disruption it caused. The shape of the two trajectories that emerge are very different: Zapatero, a popular and populist transformative leader, rapidly loses capital in a “cascade” while the right-wing, cautious delegator Rajoy preserves and incrementally increases his. Both leaders failed the ultimate electoral test, respectively ousted by their party in 2011 and winning a pyrrhic electoral majority at the polls in 2015 but unable to form a government. The comparison reveals how both leaders lacked the necessary skills, relations, and reputation for crisis management, failing to build a narrative or communicate, while also beset by distrust, and declining personal and party popularity ratings.

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18

C, Hall Kenneth, and United States. National Aeronautics and Space Administration., eds. Sensitivity analysis for aeroacoustic and aeroelastic design of turbomachinery blades: Final technical report. Dept. of Mechanical Engineering and Materials Science, School of Engineering, Duke University, 1995.

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19

TADS, a CFD-based turbomachinery and analysis design system with GUI. National Aeronautics and Space Administration, 1995.

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20

A, Myers R., Delaney R. A, and United States. National Aeronautics and Space Administration., eds. TADS, a CFD-based turbomachinery and analysis design system with GUI. National Aeronautics and Space Administration, 1995.

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21

A, Myers R., Delaney Robert A, and United States. National Aeronautics and Space Administration., eds. TADS, a CFD-based turbomachinery and analysis design system with GUI. National Aeronautics and Space Administration, 1995.

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22

Beeson, Pélagie M., and Kindle Rising. Acquired Dysgraphias: Mechanisms of Writing. Edited by Anastasia M. Raymer and Leslie J. Gonzalez Rothi. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780199772391.013.13.

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Acquired dysgraphia refers to disorders of spelling or writing due to neurological damage in individuals with normal premorbid literacy skills. Dysgraphia can result from the disruption of central cognitive processes that also support spoken language and reading, so that spelling impairments frequently co-occur with aphasia and acquired alexia. The ability to produce written words can also be affected by damage to peripheral processes necessary to plan and execute the appropriate hand movements for letter generation or typing. In this chapter, we review the cognitive processes that support spelling and writing, and the characteristic dysgraphia syndromes that reflect differential impairment to specific central and peripheral components. We also review assessment procedures for writing and spelling that are structured to clarify the status of component processes and to guide rehabilitation planning. Treatment procedures and sequences are described with a focus on lexical-semantic, phonological, and interactive treatments. The nature and treatment of dysgraphia are illustrated by case examples of global dysgraphia, phonological dysgraphia, and surface dysgraphia.

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23

Gaskell, Elizabeth, and Dinah Birch. Cranford. Edited by Elizabeth Porges Watson. Oxford University Press, 2011. http://dx.doi.org/10.1093/owc/9780199558308.001.0001.

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A man … is so in the way in the house!’ A vivid and affectionate portrait of a provincial town in early Victorian England, Elizabeth Gaskell’s Cranford describes a community dominated by its independent and refined women. Undaunted by poverty, but dismayed by changes brought by the railway and by new commercial practices, the ladies of Cranford respond to disruption with both suspicion and courage. Miss Matty and her sister Deborah uphold standards and survive personal tragedy and everyday dramas; innovation may bring loss, but it also brings growth, and welcome freedoms. Cranford suggests that representatives of different and apparently hostile social worlds, their minds opened by sympathy and suffering, can learn from each other. Its social comedy develops into a study of generous reconciliation, of a kind that will value the past as it actively shapes the future. This edition includes two related short pieces by Gaskell, ‘The Last Generation in England’ and ‘The Cage at Cranford’, as well as a selection from the diverse literary and social contexts in which the Cranford tales take their place.

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24

Makurumidze, Getrude, Anna Gamell, and Emili Letang. AIDS Orphans and Other Children Affected by HIV. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0005.

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Since the beginning of the HIV/AIDS epidemic, the number of deaths in reproductive age groups has led to nearly 18 million children being left orphaned. Orphans are not only faced with the loss of one or both parents but may also suffer loss of property and inheritance, disruption from school, and psychosocial distress from the stigma associated with HIV/AIDS. This chapter explores the psychological, social, and cultural aspects of HIV/AIDS orphanhood. It addresses the financial and emotional support that orphans and their caregivers need, as well as key strategies shown to be effective to protect, support, and empower orphans and vulnerable children (OVC). Such strategies include providing education, psychosocial care and support, household economic strengthening, social protection, health and nutrition, child and legal protection, and capacity building. However, despite the considerable progress achieved, multiple challenges still prevent many OVC from receiving effective care and support. These aspects need to be urgently addressed in order to build evidence-based programs, respond to the needs of all AIDS-affected children, and achieve the dream of an AIDS-free generation.

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25

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.

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26

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.

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Abstract:

Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

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27

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.

Full text

Abstract:

Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

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Books on the topic 'Cascade disruption of generation'

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