Courtesy CDCImagine you're the director of the
Center for Disease Control, the US government’s top job for handling public health concerns.
Suddenly you’re faced with a new strain of flu, and must make a series of decisions over the course of a year on how to handle the outbreak. What will you do? Head on over to the Science Buzz swine flu feature and play the, "Swine flu: what would you do?" simulation. Test your decision-making ability to handling a possible flu crisis. See how your decisions compare with others who’ve tried this activity.
A research group led by Dirk Brockmann at Northwestern University has created a computer model that predicts the spread of the 2009 H1N1 influenza virus in the US. (It uses a complex set of mathematical equations to describe the movement of people and virus.)
Courtesy CDC/C.S. Goldsmith and A. Balish
(Brockmann was a guest on Minnesota Public Radio's Midmorning show today, and you can listen to it online.)
The good news is that, based on what we know now, and assuming that no one takes any preventive measures, we could expect to see some 1,700 cases of swine flu in the next four weeks. Because of the preventive measures being taken wherever a suspected case of H1N1 flu has popped up, we should actually see fewer cases. (You can see Brockmann's models here.) That's lousy if you're one of the folks who picks up the virus, but not a devastating number of cases. Of course, this is a rapidly developing, fluid situation, and things may change. Still, tools like Brockmann's model help to ensure that emergency supplies and other resources get to the places likely to need them most before they're needed.
Don't have faith in computer models? Well, a second research group at Indiana University is using another model, with different equations, and getting very similar results. That's a pretty good indication that the predictions are reliable.
You might remember Brockmann from a 2006 study that used data from WheresGeorge.com, a site that allows users to enter the serial numbers from their dollar bills in order to see where they go, to predict the probability of a given bill remaining within a 10km radius over time. That gave him a very good picture of human mobility, reflecting daily commuting traffic, intermediate traffic, and long-distance air travel, all of which help to model how a disease could spread.
Most insecticides work by killing bugs before they get the chance to grow and reproduce, but a new research study suggests that when it comes to mosquitos and malaria, this strategy might be part of the problem. Killing young mosquitoes increases the selective pressure on the population to develop resistance to pesticides. This means that any given pesticide will stop working shortly after it is introduced, making it harder to fight the disease, which is caused by parasites and spread by mosquitoes. By killing the mosquitoes when they are older, but before they are old enough to spread Malaria, scientists believe they can prolong the effectiveness of pesticides and save lives. This article explains more about their ideas. Learn more about malaria and share your thoughts on Science Buzz.
OK, I think the history of infectious disease is fascinating, and I'm a sucker for many things gross, but I'm still a bit surprised that I loved this little quiz game about the bubonic plague as much as I did. You gotta play. Did you love the animation and sound effects as much as I did?
Courtesy USDA - Scott Bauer
"It's now becoming clear that some types of diseases can spread more rapidly and widely than we anticipated," said Chris Mundt, a professor of plant pathology at OSU. His research paper in The American Naturalist explains why.
"This wheat disease problem could be global within a few years," Mundt said. "We would be foolish to ignore it." (read more in Science Daily)
Courtesy Destinys Agent
(With the Republican National Convention literally across the street, the Science Museum of Minnesota will be closed starting Friday, August 29. But Science Buzz marches on! To honor our convention guests, I’ll be posting entries focusing on issues where science and politics overlap. Hopefully this will spur some discussion. Or at least tick some people off. Previous entries here and here.)
Getting a new drug approved for use is a long and arduous process. As well it should be—we need to be sure not only that the drug works, but also that it doesn’t have any nasty, even fatal, side-effects.
Unfortunately, the process has gotten slower lately. The US Food and Drug Administration is approving only half as many drugs as it did a decade ago. Some observers believe the organization has grown gun-shy. After Vioxx and a few other high-profile drugs had to be pulled from the market over safety concerns, the agency has become a lot more cautious.
(The cynical among us might say the FDA is out to protect its own skin, regardless of how many lives are lost by withholding drug approvals. At the same time, one can argue that they agency has been forced into its current cautious approach by the media and Congress, who heap criticism and blame on the FDA for its few mistakes, but never offer any praise for its many successes.)
Another issue arises from the pre-approval trials. New drugs are tested on a small number of patients. Often there are more patients interested in taking part in the trial than there are slots available. This can be especially difficult for terminally ill patients who have exhausted all other treatment options – nothing has worked, and they are still dying. They would have nothing to lose, and potentially a lot to gain, from trying an experimental drug. The drug trial itself might benefit from having more subjects. It’s win-win.
But getting such patients added to trials has proven very difficult. In May, Sen. Sam Brownback (R., Kan.) and Rep. Diane Watson (D., Calif.) introduced a bill to open up access to trials for such patients. No action was taken before Congress recessed for the summer.
Courtesy FIR0002New research coming out of Britain shows eating broccoli may reverse damage done by diabetes to heart and blood vessels. I’m always glad to hear anything new about the benefits of broccoli. Not that I have diabetes – I don’t. But broccoli is my favorite vegetable, and besides its potentially new vascular benefits, the leafy vegetable is high in fiber, full of vitamins C and K, and nutrients that have been found to reduce the risk of some cancers. A member of the cabbage family (Brassica), broccoli, along with other vegetables in the genus (including brussel sprouts, cauliflower, turnips, kohlrabi, and mustard seed) has been linked to the reduction of strokes and heart attacks.
Diabetes is a serious metabolic disorder resulting in abnormally high levels of blood sugar (hyperglycemia). The disease can affect nearly every part of the body, and left untreated can lead to blindness, kidney failure, nerve damage, and loss of limb. Diabetics have up to 5 times the risk of suffering from vascular diseases such as heart attacks, strokes because of damaged blood vessels.
The current research involves the anti-cancer compound sulforaphane, a product of another compound found in broccoli called glucoraphanin. Sulforaphane encourages production of enzymes that protect blood vessels, and reduce levels of cell-damaging molecules. When researchers at the University of Warwick tested the effects of sulforaphane on blood vessels damaged by hyperglycemia (high sugar levels), they noticed a nearly 75% reduction of Reactive Oxygen Species (ROS) molecules in the body. High levels of ROS -the result of increased blood sugar- can damage cells. The researchers noted sulforaphane also protected cells by triggering a protein that activated antioxidant enzymes.
“Our study suggests that compounds such as sulforaphane from broccoli may help counter processes linked to the development of vascular disease in diabetes,” said Professor Paul Thornalley of the University of Warwick. His team’s appears in the journal Diabetes. Thornalley added that he expects future tests of a brassica vegetable-rich diet could yield further health benefits for diabetic patients.
"It is encouraging to see that Professor Thornalley and his team have identified a potentially important substance that may protect and repair blood vessels from the damaging effects of diabetes,” said Dr Iain Frame, director of research at the charity Diabetes UK. "It also may help add some scientific weight to the argument that eating broccoli is good for you."
That brings to mind the time when the first president Bush said since he was president he didn’t have to eat broccoli anymore. (I think the quote was “Read my lips: no more broccoli”) Well, good for him. It just means more of the natural, leafy panacea for the rest of us.
Researchers at Swansea University, in the UK, are developing an antibiotic that can fight the MRSA superbug. And they're using superbugs to do it. OK, not superbugs. They're using the secretions from the maggots of the common green bottle fly.
Courtesy National Institutes of Health
Super gross? Sure. And you won't see an ad for this antibiotic (Seraticin) on TV anytime soon. It takes some 20 maggots to make a single drop of the drug. So scientists have to fully identify it, figure out a way to synthesize it in the lab, test it on human cells, and put it through a clinical trial.
In the meantime, using live maggots on infected wounds is a time-tested way of beating infections. Dr. Alun Morgan, of ZooBiotic Ltd, told the BBC,
"Maggots are great little multitaskers. They produce enzymes that clean wounds, they make a wound more alkaline which may slow bacterial growth and finally they produce a range of antibacterial chemicals that stop the bacteria growing."
How effective are maggots? The University of Manchester has been doing research on diabetic patients with MRSA-contaminated foot ulcers. The patients treated with maggots were mostly cured within three weeks. Patients who got more conventional treatment needed 28 weeks.
Next year, researchers plan to start small-scale human trials of a malaria vaccine that's proven 75-80% successful in mice.
Researchers at the International AIDS Conference sifted through published papers on the risk of heterosexual HIV transmission. They say that while a popular estimate pegs the rate of HIV transmission through heterosexual sex at 1 per 1000 contacts, true rates of infectivity are all over the map and dependent on many variables. The infectivity rate for certain sorts of activities is much, much higher-- as high as 1 in 3 contacts. The take away message? "Claims in both the popular media and the peer-reviewed literature that HIV is very difficult to transmit heterosexually are dangerous in any context where the possibility of HIV exposure exists."