Secret of Usain Bolt's speed unveiled
Scientists say they can explain Usain Bolt's extraordinary speed with a mathematical model.
His 100m time of 9.58 seconds during the 2009 World Championships in Berlin is the current world record.
They say their model explains the power and energy he had to expend to overcome drag caused by air resistance, made stronger by his frame of 6ft 5in.
Writing in the European Journal of Physics, the team hope to discover what makes extraordinary athletes so fast.
According to the mathematical model proposed, Bolt's time of 9.58 seconds in Berlin was achieved by reaching a speed of 12.2 metres per second, equivalent to about 27mph.
The team calculated that Bolt's maximum power occurred when he was less than one second into the race and was only at half his maximum speed. This demonstrates the near immediate effect of drag, which is where air resistance slows moving objects.
They also discovered less than 8% of the energy his muscles produced was used for motion, with the rest absorbed by drag.
When comparing Bolt's body mass, the altitude of the track and the air temperature, they found out that his drag coefficient - which is a measure of the drag per unit area of mass - was actually less aerodynamic than that of the average man.
Effects of drag
Jorge Hernandez of the the National Autonomous University of Mexico said: "Our calculated drag coefficient highlights the outstanding ability of Bolt. He has been able to break several records despite not being as aerodynamic as a human can be.
"The enormous amount of work that Bolt developed in 2009, and the amount that was absorbed by drag, is truly extraordinary.
"It is so hard to break records nowadays, even by hundredths of a second, as the runners must act very powerfully against a tremendous force which increases massively with each bit of additional speed they are able to develop.
"This is all because of the 'physical barrier' imposed by the conditions on Earth. Of course, if Bolt were to run on a planet with a much less dense atmosphere, he could achieve records of fantastic proportions.
"The accurate recording of Bolt's position and speed during the race provided a splendid opportunity for us to study the effects of drag on a sprinter.
"If more data become available in the future, it would be interesting to see what distinguishes one athlete from another," added Mr Hernandez.
Bolt's time in Berlin was the biggest increase in the record since electronic timing was introduced in 1968.
John Barrow at Cambridge University who has previously analysed how Bolt could become even faster, explained that his speed came in part due his "extraordinary large stride length", despite having such an initial slow reaction time to the starting gun.
"He has lots of fast twitch muscle fibres that can respond quickly, coupled with his fast stride is what gives him such an extraordinary fast time."
He said Bolt has lots of scope to break his record if he responded faster at the start, ran with a slightly stronger tail-wind and at a higher altitude, where there was less drag.
Bolt's Berlin record was won with a tail wind of only 0.9m per second, which didn't give him "the advantage of helpful wind assistance", he added.
"You're allowed to have a wind no greater than 2m per second to count for record purposes, so without becoming any faster he has huge scope to improve," Prof Barrow told BBC News.
Friday, July 26, 2013
Tuesday, July 23, 2013
HPV Vaccine Might Shield Women Against Throat Cancer: Study
Vaccination already recommended for boys and girls to guard against sexually transmitted infections
FRIDAY, July 19 (HealthDay News) -- Young women who are vaccinated against the human papillomavirus (HPV) not only protect themselves from cervical cancer, but from throat cancer as well, a new study suggests.
Many of the increasing number of throat cancers, seen mostly in developed countries, are caused by HPV infection and the HPV vaccine might prevent many of these cancers, the researchers say.
"We found the women who had the HPV vaccine had much less infection than the women who hadn't," said lead researcher Dr. Rolando Herrero, at the International Agency for Research on Cancer in Lyon, France.
"In fact, there was a 90 percent reduction in the prevalence of HPV infection in the women who received the vaccine compared to the women who had not," he said.
HPV infection is strongly associated with cancer of the oral cavity, Herrero noted. "We think that it is possible that the prevention of the infection will also lead to the prevention of these cancers," he explained.
The HPV vaccine has enormous benefit, said Herrero, "because of the cervical cancer prevention and the anal cancer prevention, and it can even prevent infections in their sexual partners."
Herrero said boys, too, should be vaccinated to protect them from oral cancers. Oral cancer is much more prevalent among men than in women, he pointed out.
A 2011 study in the Journal of Clinical Oncology showed that in the United States, HPV-positive oral cancers increased from 16 percent of all oral cancers in the 1980s to 70 percent in the early 2000s.
And according to the Oral Cancer Foundation, nearly 42,000 Americans will be diagnosed with oral and throat cancer in 2013, and more than 8,000 people will die from these conditions.
HPV-linked throat cancer recently came to the public's attention when the British newspaper The Guardian reported that actor Michael Douglas' recent bout with the disease might have been caused by oral sex.
For the new study, Herrero's team randomly assigned more than 7,400 women aged 18 to 25 to either receive the HPV vaccine or a vaccine against hepatitis A, as a comparison.
Women in the HPV vaccine group were given Cervarix, one of two vaccines available for HPV prevention. (The other is Gardasil.)
Four years later, the researchers found the HPV vaccine was 93 percent effective in preventing throat cancer. Among women who received the HPV vaccine, only one patient showed an oral HPV infection, compared with 15 in the hepatitis A vaccine group, the researchers found.
The HPV vaccine costs $130 a dose and because three shots are required, the total cost is about $390, according to the U.S. Centers for Disease Control and Prevention. There are government programs that can help offset these costs for some patients, the agency noted.
Because HPV is a sexually transmitted infection, the vaccine is most effective when given before someone is sexually active. Eighty percent of people will test positive for HPV infection within five years of becoming sexually active, said Dr. Marc Siegel, an associate professor of medicine at NYU Langone Medical Center, in New York City.
That's why the CDC recommends the vaccine for adolescent girls and boys starting at age 11.
The new report was published in the July issue of the online journal PLoS One.
"The study is really preliminary information," said Dr. Elizabeth Poynor, a gynecologic oncologist and pelvic surgeon at Lenox Hill Hospital, in New York City. "It will provide a basis to begin to study how the vaccine will help to protect against throat cancer," she noted.
"It's going to take a while to study those who have been vaccinated to determine that they are protected against throat cancer. This is just the beginning," she said.
"It also really highlights that we need to vaccinate young boys," Poynor added.
Saturday, July 20, 2013
Overweight? Maybe You Really Can Blame Your Genes
The mice were eating their usual chow and exercising normally, but they were getting fat anyway. The reason: researchers had deleted a gene that acts in the brain and controls how quickly calories are burned. Even though they were consuming exactly the same number of calories as lean mice, they were gaining weight.
So far, only one person — a severely obese child — has been found to have a disabling mutation in the same gene. But the discovery of the same effect in mice and in the child — a finding published Wednesday in the journal Science — may help explain why some people put on weight easily while others eat all they want and seem never to gain an ounce. It may also offer clues to a puzzle in the field of obesity: Why do studies find that people gain different amounts of weight while overeating by the same amount?
Scientists have long thought explanations for why some people get fat might lie in their genes. They knew body weight was strongly inherited. Years ago, for example, they found that twins reared apart tended to have similar weights and adoptees tended to have weights like their biological parents, not the ones who reared them. As researchers developed tools to look for the actual genes, they found evidence that many — maybe even hundreds — of genes may be involved, stoking appetites, making people voraciously hungry.
This rare gene-disabling mutation, though, is intriguing because it seems to explain something different, a propensity to pile on pounds even while eating what should be a normal amount of food. Investigators are now searching for other mutations of the same gene in fat people that may have a similar, but less extreme effect. The hope is that in the long term, understanding how this gene affects weight gain might lead to treatments for obesity that alter the rate at which calories are burned.
“The history of obesity for many many years has been one of blaming people for lack of self control,” said Dr. Joseph Majzoub, chief of endocrinology at Boston Children’s Hospital and lead author of the new paper. “If some of it is due to a slow metabolism, that would completely change the perspectives of parents and patients. It really would change the way we think of the disease.”
In their paper, Dr. Majzoub and his colleagues describe figuring out how the gene they deleted, known as MRAP2, acts in the brain to control weight. They discovered that it is a helper gene. It normally acts in the brain to signal another gene already known to be involved in controlling appetite. So they developed a hypothesis. If the helper gene was deleted, the brakes should come off the gene that controls appetite. Animals should eat voraciously.
The first thing they noticed was that the mice got fat, ending up weighing twice as much as their normal siblings, with most of that extra weight due to fat accumulation.
“During the mouse equivalent of childhood and adolescence they were becoming rapidly obese,” Dr. Majzoub said.
The surprise came when the researchers figured out why. When the mice were young, they had normal appetites. The researchers measured what they and their normal siblings ate and determined they were eating the same amount of food. Yet the mice with the deleted gene still gained weight. The only way the obesity-prone mice could be kept slim was to be fed 10 to 15 percent less than their siblings.
But as adults, the mice with the missing gene developed monstrous appetites. Given a chance, they ate much more than their siblings, exacerbating the effects of their tendency to turn food into fat.
That led the researchers to ask if the same genetic phenomenon could be making people obese. They contacted Dr. Sadaf Farooqui of the University of Cambridge, whose group has been mapping the genes of massively obese children, and studied the data on 500 of the children, searching for mutations that disabled the same gene they had deleted in mice.
One child clearly had a gene-disabling mutation and three others had mutations that the investigators suspect might render the gene nonfunctional. None of the normal-weight children who served as controls had a mutation in the helper gene.
“From a basic science point of view, this is really interesting and exciting,” said David Allison, an obesity researcher at the University of Alabama in Birmingham who was not involved in the study. Any discovery that helps fill in the details of how the brain controls eating and weight gain is important, he added.
Jeffrey Friedman, an obesity researcher at Rockefeller University, who also was not involved in the study, said, “It is another piece in a very important puzzle.”
The work fascinates Claude Bouchard, a genetics researcher at the Pennington Biomedical Research Center in Baton Rouge, La., because it might offer insight into an intriguing finding: there are genetic controls not just of how much people want to eat but also how much of what they eat turns into fat or is burned off and not used by the body. Although the common mantra is that a calorie is a calorie and 3,500 extra calories eaten equals a pound of fat on the body, that is not what happens in real life, he found.
For example, in one of his studies, Dr. Bouchard enlisted 12 pairs of lean identical twins to live in an enclosed area for 120 days so their food and exercise could be monitored while they ate 1,000 calories a day more than needed to maintain their weight. The twins in each pair gained about the same amount of weight, but the amount gained varied threefold among the pairs. Those who gained the most put on as much as 29 pounds while those who gained the least put on 9 ½ pounds.
“It is not a freak finding,” Dr. Bouchard said, adding that about 20 studies found the same threefold range in weight gain in response to excess calories. But it also is not clear why this occurs. The intriguing possibility, he said, is that the newly discovered gene might be among those involved. The level of its activity might help determine how quickly calories are burned.
Dr. Majzoub and his colleagues are now trying to determine whether additional mutations in the gene they discovered — ones that hinder its function but do not completely disable it — might explain why some people gain weight.
“All we can do is hope,” Dr. Majzoub said.