The dynamic interactions between cellular-molecular physiology and the environment - case studies in pathophysiology - how to exploit cellular-molecular evolution

Published on May 31, 2016   8 min

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My name is John Torday. I am a professor of evolutionary medicine at UCLA. This lecture is entitled Case Studies in Pathophysiology, how to exploit cellular-molecular evolution.
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Many chronic diseases are characterized by a simplification of structure and function. This simplification process is associated with the loss of differentiated growth factor receptor signaling and a gain of signaling characteristic of an earlier developmental and/or phylogenetic phase. This phenomenon is traditionally interpreted as inflammation, because it is associated with scarring. Such data also suggests a regression of the tissue towards an earlier stage in its evolution, the inflammation resulting from loss of homeostatic control as a result, not a cause of the disease. If that is that case, then in theory, structure and function could be restored by driving the tissue back in the forward direction to reestablish homeostasis and effectively treat disease.
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For example, chronic lung disease induced by oxygen exposure is associated with simplification, as shown by the histograms on the far right measuring alveolar septation and wall thickness. On the right is shown the increase in Wingless/Inter "Wnt" signaling in the alveoli characteristic of both inflammation and simplification of the lung. Treatment with an anti-inflammatory agent, such as curcumin, normalizes this condition.
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The dynamic interactions between cellular-molecular physiology and the environment - case studies in pathophysiology - how to exploit cellular-molecular evolution

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