August 7, 2009
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Gut Check I: A novel function for the gut hormone cholecystokinin (CCK) was discovered by Tony Lam’s research team at the Toronto General Research Institute and made the cover story in Cell Metabolism this week. Activation of the CCK hormone sends a signal to the brain and then to the liver to trigger lower sugar production. However, resistance to CCK occurs following high-fat feeding and corresponds to elevated blood sugar levels. This work follows a series of ground-breaking discoveries by Tony Lam’s group over the last few years identifying a novel gut-brain-liver neuronal circuitry regulating glucose production, which presents an alternate approach to combating obesity and diabetes.
Gut Check II: There are trillions of friendly bacteria in our lower intestines that play an important role in maintaining a healthy gastrointestinal system. Our innate immune system, which includes Toll-like receptor signaling, detects and keeps these microbes compartmentalized in the gut. But what would happen if this innate immune system is compromised? A study published in this week’s issue of Science by Dr. AJ Macpherson at McMaster University used a mouse model deficient in innate immune responses (i.e. lacking Toll-like receptors) to demonstrate that intestinal bacteria escapees into the body trigger a cooperative response from the adaptive immune system (e.g. antibodies) to compensate and maintain the host-bacteria mutualism.
My Space – for Stem Cells: Stem cells need their personal space too. Some important signaling pathways are regulated by the size of the colony and niche and can influence stem cell fate. Peter Zandstra’s Stem Cell Bioengineering Lab at the University of Toronto completed an intricate study that defined the spatial parameters of the stem cell microenvironment and hinted that these factors should be considered when planning experiments and interpreting results.
Muscle wasting in Cystic Fibrosis: Patients with Cystic Fibrosis usually experience muscle atrophy and it was previously thought to be a secondary effect of the disease. New evidence presented in this PLoS – Genetics article by Dr. Basil Petrof’s group at McGill University Health Centre shows that muscle loss may be predisposed, a direct symptom of mutations in the CFTR gene in muscle cells. In addition to abnormal calcium levels, CFTR-deficient muscle cells exhibit an elevated inflammatory response and upregulation of genes associated with protein degradation or muscle atrophy. These results have implications for current treatments to more aggressively control inflammation and target calcium homeostasis.
May 29, 2009
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Interestingly, my PubMed Canadian publications search this week turned up three articles about infectious diseases (and a Science paper about astronomy that I will spare you my attempts to describe). Check out this week’s Canadian accomplishments: showing that group adaptation is just selfishness after all, plus new ways in which staphylococci and HIV each find sneaky ways to monkey with the immune system, after the jump…