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Books on the topic 'Apoptosis/Necrosis'

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Author: Grafiati

Published: 11 March 2023

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1

Ennis, Maurice. Tumour necrosis factor alpha and ultraviolet light activation of programmed cell death by apoptosis in D. melanogaster. Ottawa: National Library of Canada, 2001.

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2

C, Hemmings Hugh, ed. Regulatory protein modification: Techniques and protocols. Totowa, N.J: Humana Press, 1997.

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3

service), SpringerLink (Online, ed. Death receptors and cognate ligands in cancer. Heidelberg: Springer, 2009.

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4

Ntuli, Tobias M., ed. Cell Death - Autophagy, Apoptosis and Necrosis. InTech, 2015. http://dx.doi.org/10.5772/59648.

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5

Aerts, Joeri. Progesterone Induces Apoptosis in Eosinophilic Granulocytes & Induces Tumour Necrosis Factor-Alpha / Tumour Necrosis Factor Receptor. Leuven Univ Pr, 2002.

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6

Dynamic changes in cell death after lung transplantation: Apoptosis and necrosis in ischemia-reperfusion injury. Ottawa: National Library of Canada, 2000.

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7

(Editor), N. G. Bazan, U. Ito (Editor), V. L. Marcheselli (Editor), T. Kuroiwa (Editor), and I. Klatzo (Editor), eds. Maturation Phenomenon in Cerebral Ischemia IV: Apoptosis and/or Necrosis, Neuronal Recovery vs. Death, and Protection Against Infarction. Springer, 2001.

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8

Klatzo, I., T. Kuroiwa, U. Ito, N. G. Bazan, and V. L. Marcheselli. Maturation Phenomenon in Cerebral Ischemia IV: Apoptosis and/or Necrosis, Neuronal Recovery vs. Death, and Protection Against Infarction. Springer London, Limited, 2012.

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9

Maturation Phenomenon in Cerebral Ischemia IV: Apoptosis and/or Necrosis, Neuronal Recovery vs. Death, and Protection Against Infarction. Springer, 2011.

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10

Bahjat, Frances Rena. Characterization and genetic analysis of the resistance of nonobese diabetic mice to tumor necrosis factor-alpha-mediated hepatocyte apoptosis and lethality. 2002.

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11

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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12

Regulatory Protein Modification: Techniques and Protocols. Humana Press, 2010.

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13

Death Receptors in Cancer Therapy (Cancer Drug Discovery and Development). Humana Press, 2004.

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14

Kalthoff, Holger. Death Receptors and Cognate Ligands in Cancer. Springer, 2012.

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15

Yilmaz, Ali, and Anca Florian. Myocarditis: imaging techniques. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0367.

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The clinical presentation of myocarditis is multifaceted and electrocardiogram (ECG) changes as well as biomarkers tend to be non-specific. Therefore, the diagnosis of myocarditis can be challenging and should be based on an integrated approach including patient history, physical examination, non-invasive tests such as ECG and serum biomarkers, and non-invasive cardiac imaging. As myocarditis may lead to global ventricular dysfunction, regional wall motion abnormalities, and/or diastolic dysfunction, echocardiography should be routinely performed. However, hallmarks of acute myocarditis comprise structural changes such as cardiomyocyte swelling, an increase in extracellular space and water content, accumulation of inflammatory cells, potential necrosis or apoptosis of cardiomyocytes, and myocardial remodelling with fibrotic tissue replacement that can be depicted by cardiovascular magnetic resonance. Nuclear techniques are still not routinely recommended for the work-up of myocarditis—with the possible exception of suspected sarcoidosis—due to limited data, limited diagnostic specificity, limited availability, and risk from radiation exposure. This chapter focuses on those non-invasive cardiac imaging techniques that are used in daily clinical practice for work-up of suspected myocarditis. However, as research continues and novel imaging techniques become available, it is hoped that even more accurate and timely diagnosis of myocarditis will be possible in the near future.

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16

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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