Canada geese fly in a V-formation to save energy.
CBC.CA
September 21, 2009
by Sharon Oosthoek
Bird migration looks like a bad idea at first glance — all that energy needed to fly thousands of kilometres, all those predators along the way and the promise of doing it all over again just a few months later.
But of course Mother Nature knows exactly what she is doing. If you’ve ever wondered, as we did, what all that back and forth across the sky is about, read on.
CBC.CA
September 19, 2009
By Sharon Oosthoek
A centimetre-long wasp is poised to become a lead investigator of potential infestations by emerald ash borers, a beetle that is destroying swaths of trees across eastern North America.
Researchers at Ontario’s University of Guelph say Cerceris fumipennis — a wasp native to the region — can determine in as little as half an hour after leaving its nest in search of prey whether the invasive beetles are in the area.
Cerceris fumipennis wasp with its beetle prey. This native wasp can determine in as little as 30 minutes if emerald ash borers are in the area. (Mike Bohne/U.S. Department of Agriculture Forest Service)
Traditional sleuthing involves peering into treetops where beetles congregate, or hanging sticky traps. But both are costly and finding the beetles can take days, weeks, or even years if the infestation is in the very early stages.
Yet the earlier an infestation is discovered, the fewer trees have to be cut down or injected with expensive pesticides to stop the beetles’ spread.
Now some U.S. forest managers in New England and New York state are pressing this black-winged wasp into service, and the Canadian Food Inspection Agency (CFIA) is seriously considering following suit.
Alzheimer Society of Ontario website
September 2009
The possibilities for human genetic variation surpass 10 million, yet it’s Dr. Ekaterina Rogaeva’s job to track down the ones that boost our risk of Alzheimer’s disease.
“Our main task as geneticists is to ask, ‘Is it a guilty or innocent variation?’ says Dr. Rogaeva, a researcher with University of Toronto’s Centre for Research in Neurodegenerative Diseases. “Then we have to ask, ‘Is it enough to have the variation to cause Alzheimer’s disease, or does it act only in combination with other factors?’”
Ekaterina Rogaeva in her lab. (Photo by Steve McKinley)
Despite the mind-boggling challenge, Dr. Rogaeva was instrumental in figuring out that a mutated form of the gene SORL1 increases the risk of late-onset Alzheimer’s disease by 10 to 20 per cent.
SORL1 directs the traffic of amyloid precursor protein (APP) inside nerve cells of the brain.
When the gene is working properly, it diverts APP into certain areas of the cell. But in its mutated form, the gene tells APP to accumulate in a different region of the cell, where it degrades into abnormal protein fragments responsible for Alzheimer’s disease.
Dr. Rogaeva and her team sifted through 6,000 DNA samples to uncover the risk involved in carrying this particular variation of SORL1.
She also helped discover the mutated form of two presenilin genes – PS1 and PS2 – responsible for the most aggressive early-onset form of the disease.
While neither breakthrough has immediate implications for those suffering from Alzheimer’s disease, it will be meaningful to those at risk for the debilitating disease in the future.
“Once treatment is available – and I believe we will have treatment, there are so many people working on it – early diagnosis will be extremely important,” says Dr. Rogaeva.
That’s because most people are diagnosed only after the disease has progressed and many brain cells have already died. Once these cells are dead, there is nothing for the drug to treat.
Identifying genes that increase the risk of Alzheimer’s is also important in more direct ways. “It gives us another therapeutic target,” says Dr. Rogaeva. “Can we fix the gene? That work is going on in this centre right now.”
In the meantime, she continues to investigate other potential genetic links to neurodegenerative disease.
Dr. Rogaeva is currently working with researchers at Columbia University in New York to analyze complete genetic scans of 1,000 people to pinpoint more guilty variations. She is also investigating possible genetic links between Alzheimer’s disease and other neurodegenerative illnesses such as Parkinson’s disease and frontal temporal dementia.
“Thirty per cent of people with Parkinson’s disease end up having Alzheimer’s disease. Is there a common genetic factor, or is it just the way disease progresses as people lose brain cells?” she says, clearly eager to get to the bottom of it.
“It’s never boring. I love this job.”
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