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1
Bromfield, Gillian. Cell death pathways in irradiated prostate cells. Ottawa: 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, accompanied by changes in the microcirculation. Although all renal resident cells participate in AKI, the brunt falls on the epithelial and endothelial cells, the fact that underlies the development of tubular epithelial and vascular compromise.This chapter further summarizes the involvement of several cell organelles in AKI: mitochondrial involvement in perturbed energy metabolism, lysosomal involvement in degradation of misfolded proteins and damaged organelles, and peroxisomal involvement in the regulation of oxidative stress and metabolism, all of which become defective. Common molecular pathways are engaged in cellular stress response and their roles in cell death or survival. The diverse families of nephrotoxic medications and the respective mechanisms they induce AKI are discussed. The mechanisms of action of some nephrotoxins are analysed, and also of the preventive therapies of ischaemic or pharmacologic pre-conditioning.An emerging concept of the systemic inflammatory response triggered by AKI, which can potentially aggravate the local injury or tend to facilitate the repair of the kidney, is presented. Rational therapeutic strategies should be based on these well-established pathophysiological hallmarks of AKI.
6
Anning, Lin, ed. The JNK signaling pathway. Georgetown, Tex: 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 downplayed the role of context in cancer progression, and the fact that disorderly cellular growth is affected by many pathways. I conclude by considering several philosophers’ accounts of “causal selection” and argue that ultimately the causal selection problem is not one but several different problems, requiring different, context-specific solutions.
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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 potential use in therapy has not yet been shown. However, the analysis of embryonic renal stem cells, specifically stem/progenitor cells that are induced into the nephrogenic pathway to form nephrons until the 34th week of gestation, has been much more conclusive.
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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 dysfunction is closely associated with proteinuria, which in turn is strongly associated with progressive loss of glomerular filtration rate. Continuing podocyte damage and loss could therefore account for progressive renal disease. In this hypothesis, drugs that protect against progression of renal disease may have their primary protective effects on podocytes themselves, rather than or as well as on haemodynamic factors or on fibrotic processes.
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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, TNF, and IL-23/IL-17. In experimental as well as in human SpA, the importance of these cytokine pathways are confirmed by effective reduction of signs and symptoms upon blockade of specific molecules. In-depth cellular and molecular analysis of the target tissue identifies a contribution of cells with strong innate features, rather than cells of the adaptive immune system.
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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 understood within a process-ontological framework. This framework emphasizes the interactions and mutual stabilizations between processes at different levels and this, in turn, explains the difficulty in allocating the neoplastic process to any particular level (genetic, epigenetic, cellular, or histological). Understanding these interactions is likely to be a precondition of a proper understanding of how these mutual regulations are disrupted in the processes we call cancerous.
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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% are epithelial in origin. Risk factors best confirmed to increase risk of ovarian cancer include age and a family history of ovarian cancer, while parity, oral contraceptive use, and tubal ligation decrease risk. Several etiologic pathways, including hormonal and inflammatory pathways, have garnered substantial support from both epidemiologic and laboratory studies, although many questions remain.
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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. TSC results from hyperactivation of the mammalian target of rapamycin (mTOR) pathway in neurons in the brain. This chapter reviews the clinical presentations of TSC as well as diagnostic approaches for epilepsy and SEGAs. It discusses the genetics and cellular pathogenesis of TSC as well as reviewing the link to mTOR signalling. This chapter also presents evidence for different treatment modalities for seizures and SEGAs. It is written for qualified specialist physicians and caregivers.
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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, there are likely mechanisms involved in the initiation of motor neuron loss and mechanisms involved in the progression of motor neuron loss once initiated. Our task is to determine those mechanisms that are relevant to ALS pathogenesis that may be targeted therapeutically to prevent onset and/or halt progression.
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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 at a whole-genome level. Here we describe the key molecular and cellular characteristics of the inflamed synovium and how infiltrating cells get there. With this background, we outline current concepts of the different phases of disease, how the first phase of genetic susceptibility evolves into autoimmunity, triggered by the exposome, prior to the onset of clinically apparent inflammatory disease. We then describe the pathways that actively contribute to this early inflammatory phase and document the key effector cells and molecules of the innate and adaptive immune systems that orchestrate and maintain chronic synovial inflammatory responses. We summarize how this inflammatory milieu translates to cartilage destruction and bone resorption in synovial joints, and conclude by reviewing those factors in inflamed synovium that promote immune homeostasis.