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Books on the topic 'Cell death pathways'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 February 2022

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1

Bromfield, Gillian. Cell death pathways in irradiated prostate cells. National Library of Canada, 2002.

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2

Aft, Rebecca, ed. Targeting New Pathways and Cell Death in Breast Cancer. InTech, 2012. http://dx.doi.org/10.5772/1744.

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3

(Editor), Jochen Schacht, Arthur N. Popper (Editor), and Richard R. Fay (Editor), eds. Auditory Trauma, Protection, and Repair (Springer Handbook of Auditory Research). Springer, 2008.

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4

Phosphoinositide 3-kinase Signalling Pathway: The Key to Cell Proliferation And Death. Imperial College Press, 2006.

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5

Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi, and Brian B. Ratliff. Pathophysiology of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0221.

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In the intricate maze of proposed mechanisms, modifiers, modulators, and sensitizers for acute kidney injury (AKI) and diverse causes inducing it, this chapter focuses on several common and undisputable strands which do exist.Structurally, the loss of the brush border, desquamation of tubular epithelial cells, and obstruction of the tubular lumen are commonly observed, albeit to various degrees. These morphologic hallmarks of AKI are accompanied by functional defects, most consistently reflected in the decreased glomerular filtration rate and variable degree of reduction in renal blood flow, a

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6

Anning, Lin, ed. The JNK signaling pathway. Landes Bioscience, 2006.

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7

Plutynski, Anya. Causation, Causal Selection, and Causal Parity. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780199967452.003.0004.

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It is typical to refer to cancer as a “genetic” or “genomic” disease. This claim is ambiguous; one of the central goals of this chapter is to disambiguate this claim. I first distinguish different types of causal claims: claims about causal relevance, causal role, and causal specificity. As a backdrop to this discussion, I introduce what I call the “mechanistic research program” in cancer, according to which progression to cancer involves breakdowns in regulatory controls on gene expression in ways that affect cell birth and death. While this research program has been successful, it has downpl

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8

Pleniceanu, Oren, and Benjamin Dekel. Kidney stem cells. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0344.

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End-stage renal failure is a major cause of death with currently only dialysis and transplantation available as therapeutic options, each with its own limitations and drawbacks. To allow regenerative medicine-based kidney replacement therapies and due to the fact that neither haematopoietic stem cells nor mesenchymal stem cells, the most accessible human stem cells, can be used to derive genuine nephron progenitors, much attention has been given to finding adult renal stem cells. Several candidates for this have been described, but their true identity as stem or progenitor cells and their pote

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9

Kriz, Wilhelm. Podocyte loss as a common pathway to chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0139.

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Experimental studies show that podocyte death first causes focal scars, but beyond approximately 40% loss is lethal to a glomerulus. Podocytes have limited ability to regenerate, although some degree of replacement may occur from stem cells located near the urinary pole of Bowman’s capsule. It is not yet known whether this plays a significant part in ameliorating damage in disease processes. In one interpretation, foot process effacement may be seen as an adaptation by the podocyte to remain attached to the glomerular basement membrane after injury, at the expense of proteinuria. Podocyte dysf

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10

Noordenbos, Troy, and Dominique Baeten. Immune mechanisms: innate immunity. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0007.

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Innate immune mechanisms are strongly implied in the pathophysiology of spondyloarthritis (SpA). This chapter discusses available data on the role of the innate immune system in relation to HLA-B27, genetic associations, and the cellular and molecular characteristics of disease target tissue. Regarding the linkage with MCH-class I molecule HLA-B27, the chapter discusses the arthritogenic peptide hypothesis and three popular antigen-independent theories. The genetic architecture of the disease argues against a role for the adaptive immune system and identifies cytokine pathways, such as IL-1, T

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11

Bertolaso, Marta, and John Dupré. A Processual Perspective on Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198779636.003.0016.

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This chapter attempts to illuminate the dynamic stability of the organism and the robustness of its developmental pathway by considering the biology of cancer. Healthy development and stable functioning of a multicellular organism require an exquisitely regulated balance between processes of cell division, differentiation, and death (apoptosis). Cancer involves a disruption of this balance, which results in unregulated cell proliferation. The thesis defended in this chapter is that the coupling between proliferation and differentiation, whether normal or pathological (as in cancer), is best un

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12

Tworoger, Shelley S., Amy L. Shafrir, and Susan E. Hankinson. Ovarian Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0046.

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Worldwide, ovarian cancer is the seventh most commonly diagnosed cancer and the eighth most common cause of death from cancer. In 2012, 239,000 women were diagnosed with ovarian cancer and 152,000 women died of the disease worldwide. In the United States in 2015, an estimated 21,290 women were newly diagnosed with ovarian cancer and 14,180 died from the disease. Both incidence and mortality have decreased over time in the United States, with a 1.6% and 2.1% annual decrease, respectively, from 2003 to 2012. Ovarian cancers can arise from epithelial, germ, or stromal cells, although about 90% ar

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13

Weiner, Howard, and Peter B. Crino. Familial tumour syndromes: tuberous sclerosis complex. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0017.

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Tuberous sclerosis complex (TSC) is a multisystem, genetic disorder that results from mutations in TSC1 or TSC2 genes. Neurological and neuropsychiatric disabilities include epilepsy, intellectual disability, autism, attention deficit disorder, and generalized anxiety. Cortical dysplasias (also known as tubers) are developmental abnormalities of the cerebral cortex that are believed to be responsible for seizures, cognitive disability, and autism. Subependymal giant cell astrocytomas (SEGAs) are intraventricular tumours that can cause hydrocephalus, increased intracranial pressure, and death.

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14

Ferraiuolo, Laura, and Stephen J. Kolb. Amyotrophic Lateral Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0026.

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An overriding mystery of ALS pathogenesis orbits around the molecular basis of selective motor neuron vulnerability and clouds our view. There are likely mechanisms involved in the initiation of motor neuron loss and mechanisms involved in the progression of motor neuron loss once initiated. Motor neuron vulnerability is likely related to the unique biological characteristics of these cells. This chapter introduces central molecular pathways that appear to be involved in the pathogenesis of ALS, and highlights why dysregulation of these mechanisms could lead to motor neuron death. Indeed, ther

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15

Thomas, Ranjeny, and Andrew P. Cope. Pathogenesis of rheumatoid arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0109.

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In depth molecular and cellular analysis of synovial tissue and fluid from patients with rheumatoid arthritis has provided important insights into understanding disease pathogenesis. Advances in the 1980s and 1990s included modern cloning strategies, sensitive and specific assays for inflammatory mediators, production of high-affinity neutralizing monoclonal antibodies, advances in flow cytometry, and gene targeting and transgenic strategies in rodents. In the 21st century, technological platforms offer unparalleled opportunities for systematic and unbiased interrogation of the disease process

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