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This book was originally published as: Rodan D. Disability, obesity and ageing: Popular media identifications. Farnham, England: Ashgate. Original book available here. Disability, Obesity and Ageing offers an engaging account of a new area of pressing concern, analysing the way in which 'spurned' identities are depicted and reacted to in televisual genres and online forums. From the lens of a non-survivor ally who is also a journalist, activist, sister, and educator, I offer a reflexive account of reconciling with failed media activism.

Skip to main content Skip to main navigation menu Skip to site footer. Keywords: Disability, journalism, culture industry, survivor narratives, institutionalization. Abstract From the lens of a non-survivor ally who is also a journalist, activist, sister, and educator, I offer a reflexive account of reconciling with failed media activism. References Adams St. Pierre, E. Barry, D. The boys in the bunkhouse. The New York Times. Boyer, J. House of Commons. Standing Committee on Status of Disabled Persons. Buck, G. Finding a place.

Huronia: Pierre Burton warned us 50 years ago. The Toronto Star. Cripping cyberspace: A contemporary visual art exhibition curated by Amanda Cachia. Canadian Journal of Disability Studies, 2 4. Canadian Broadcasting Corporation , February 6. The economic benefits of hiring disabled employees. Collins, K.

A message to the well intentioned [Online blog post]. Representations of disability in the Canadian new media: A decade of change? Disability and Rehabilitation, 35 22 , Disability Rhetoric. Syracuse: Syracuse University Press.

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The History of Sexuality: Volume 1. Hurley, New York: Random House. The abnormals.

Aging with an Intellectual and Developmental Disability (16 Minutes)

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New York: Columbia University Press. Seeing the disabled. Umansky Eds. New York: University Press. Integrating disability, transforming feminist theory. Davis Ed. The myth of transition: Contractualizing disability in the sheltered workshop. Global Edmonton.

The Globe and Mail Style Guide. Previously, we identified a series of genetic variations that influence the timing of sleep in humans, and mouse models of these mutations mostly recapitulate the phenotypes. Timing of sleep is heavily influenced by the circadian clock, which has been intensely studied, and we now have a large and growing body of knowledge on how the clock is regulated at the molecular level. On the other hand, our understanding of sleep homeostasis regulation for human lags behind. We reported a mutation in the human DEC2 gene that causes mutation carriers to sleep 6 hours nightly for their entire lives without apparent negative effects.

Another mutation in DEC2 was later reported in a single individual who is a short sleeper and resistant to sleep deprivation. Identification of additional genes participating in modulation of human sleep duration provides a unique way to expand our knowledge of genes and pathways critical for human sleep homeostasis regulation. Noradrenergic signaling in the central nervous system CNS has long been known to regulate sleep. The network involving the noradrenergic neurons has been extensively studied, and most of the receptor subtypes have been genetically defined.

Engineering the human mutation into mice resulted in a sleep phenotype similar to that seen in familial natural short sleepers. Also, the activity of these neurons was altered in mice harboring the mutation. The lymphatic system a part of the broader circulatory system and has many similarities to the cardiovascular system of blood vessels.

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The lymphatic system is also a network of vessels, transporting various necessary cells and substances, and subject to processes of aging that degrade function and thereby cause issues. While circulation of fluid is an important function of the lymphatic system, and conditions such as lymphedema arise when it runs awry, the role of lymphatic vessels in the function of the immune system is arguably far more vital. Immune cells must be able to rapidly travel the body and locally coordinate with one another in order to mount an effective immune response.

The lymphatic system links repositories of immune cells, such as those of the spleen and thymus with tissues throughout the body. Lymphatic vessels also link the numerous lymph nodes of the body, where immune cells gather to secrete and accept signals necessary to the correct function of the immune response. With aging, lymph nodes in particular degenerate and become fibrotic , making it ever harder for immune cells to mount an acceptable defense against pathogens and cancers.

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The presence of senescent cells and the chronic inflammation they produce is thought to be important in this process, but it is likely one of a number of contributing factors. Further, lymphatic vessels suffer problems arising from loss of control over permeability, regarding what can pass through the vessel walls, as well as many of the same issues with stiffening that are seen in aged blood vessels.

This latter problem results from processes such as cross-linking that reduces elasticity by restricting the motion of the complex molecules making up the extracellular matrix , and dysfunction of the smooth muscle tissue responsible for contraction and dilation. The aging process induces changes in structure and function of lymphatic networks. Lymphatic-related diseases are prevalent in elderly, such as lymphedema. In s, the specific "varicose bulges" in muscular lymphatic vessels were observed and this bulges were increased with age.

Muscle cell atrophy, elastic elements destruction, and aneurysm -like formations were also found in aged lymphatic vessels. Aging associated alterations in lymphatic contractility decrease pump efficiency which result in excessive retention of tissue fluid within interstitial spaces. Reduced responsiveness to inflammatory stimuli in aged lymphatic vessels decreases the normal capacity to react against foreign organisms.

The occurrence of high permeability is caused by the loss of glycocalyx and the dysfunction of junctional proteins. The lymphatic endothelial cell surface is covered by the glycocalyx layer on the lumen side. The glycocalyx functions as a barrier between lymphatic fluid and the endothelium to prevent immune cells and pathogens from adhering to the endothelium.

A significant loss of glycocalyx with a reduction in thickness and destruction in continuity occurs in lymphatic endothelial membranes from aged rat. This observation was in contrast with the intact, continuous layer covering cell membranes from adult lymphatic vessels. The global proteomic analysis of ultrastructural changes of glycocalyx composition also demonstrated a dramatic difference between the adult and aged groups.