Of sports played on ice, hockey tends to get the most attention when it comes to injuries. But figure skaters are also pretty injury-prone, and because of the aesthetic nature of their sport, most figure skaters eschew pads and protective gear while on the ice. This means avoiding injuries can be difficult for practitioners of the sport, in which skaters can exert forces of more than six times their body weight during a jump.
Figure skaters have been pushing for updated equipment (especially boots, the part of the skate that encases the feet) for some time, as injuries over the past few decades have soared. In a Wall Street Journal article from 2006, orthopedist Leisure Yu noted that skate makers were still using designs from the 1800s. Unfortunately, it doesn't seem like much has changed, and there isn't a ton of data out there about figure skating injuries -- until now. In a new study in the journal Measurement Science and Technology, researchers describe a new way to measure the stresses of figure skating. They have figured out how to build an ice skating blade (pictured below) that directly measures the impact a skating routine can have on an athlete's body.IOP Publishing/Measurement Science and Technology
"Questions have been raised about boot design and how it affects a skater's impact forces, potentially causing injuries. However, very little is known about the actual impact forces on ice during jumping and other figure skating skills, "co-author Deborah King said in a statement. "This is because on-ice measurements of the forces associated with figure skating are fairly difficult to record due to the complexity of the sport and not wanting to interfere with the skater during their jumps. As such, we decided to develop a method that measures forces directly from the blade."
The sensors themselves are attached to the part of the skate that connects the blade holder to the boot. When force is applied to the blade (like when a skater lands a jump) the system records and calculates the overall force. The entire sensor system weighs less than a third of a pound and is designed not to touch the ice or interfere with a skater's movement. The researchers plan to further refine the instruments so that in the future, the device could be used by skaters to analyze their movement during their routines and hopefully prevent further injuries.
Now a group of scientists are decoding the mystery surrounding this bizarre disorder. By mapping the genome of each individual in the Pakistan family, researchers from Uppsala University in Sweden identified a single genetic mutation responsible for the condition. Known as ITPR2, the gene is responsible for controlling sweat production, and knocking it out can stop sweat secretion altogether.
Lead researcher Niklas Dahl stumbled upon the rare family in his quest for understanding single-gene diseases, also known as Mendelian disorders. Dahl notes that anhidrosis has been seen before, but usually in conjunction with other skin defects. This family is the first he knows of to have anhidrosis as a primary isolated defect."Sweat glands made us develop this capability of walking and jogging for miles and miles without stopping."
After analyzing the genomes of the family members, Dahl and his team zeroed in on the culprit, ITPR2, which encodes a protein called IP3R2. This protein forms a calcium channel in the brain that releases calcium when opened, triggering a chain of events in the body that eventually result in sweat secretion. “In the brain, you have temperature sensitive cells, and they send signals to the nervous system, which send signals to the periphery, then to skin and to the sweat glands, and that induces sweating,” Dahl, a genetics expert at Uppsala, tells Popular Science.
For the members of the Pakistan family, their calcium channels never open. The researchers further demonstrated this defect by creating a series of genetically engineered mice without any IP3R2 production. Sure enough the rodents had reduced sweating.
Understanding the mechanisms behind sweating can actually help researchers develop drugs to reduce excessive sweating, a condition that affects two percent of the population. People with this disorder, called hyperhidrosis, start sweating in their palms, soles of their feet, chest, armpits, and other areas of the body without any provocation. Some patients will even wear plastic underneath their clothing to avoid an embarrassing situation.
Botox has proven to be somewhat effective against hyperhidrosis, but the treatments can be painful and awkward (getting injections in your armpits cannot be fun). Dahl says that lowering IP3R2 protein levels may be a much simpler solution. "We have found a way to inhibit production of this calcium channel," Dahl says. "It is targeted and very specific at least from a design point of view. We can reduce peripheral sweating by 60 percent."
Dahl also says their research highlights just how important our pungent skin secretions are from an evolutionary perspective. Humans have the highest capacity for sweating on Earth, in relation to our body size and lack of hair. This gives us the advantage of being able to exercise for very long periods of time -- up to 10 hours a day.
"Fast animals run faster than us, but they can only run for a few minutes. For humans, we could move over enormous areas because of this ability, making us very good hunters,” says Dahl. "Sweat glands made us develop this capability of walking and jogging for miles and miles without stopping."
So thank you, sweat, for helping to keep us at the top of the food chain.
The researchers published their work in the Journal of Clinical Investigation.
But how much can a viral campaign actually propel medical research? Does slacktivism advance science in a meaningful way? ALS, also known as Lou Gehrig's disease, kills off the motor neurons that control voluntary muscles. Next comes paralysis, and then death in as few as a couple of years. Even after decades of study, scientists still don't fully understand its biological mechanisms. Treatment is palliative. A cure remains a pipe dream.
Government funding for ALS research is limited, so few scientists are drawn to it, making progress slow. This new influx of funds could attract a wave of researchers to the field, says Joe Beckman, a biochemist at Oregon State University. Exploring ALS from fresh angles increases the odds of a breakthrough.
How the nonprofit will divvy up the money remains to be seen, and it's unlikely that $100 million will lead to a cure for such a mysterious disease. But "it's dramatic how science can be influenced by the public," says Su-Chun Zhang, a neuroscientist at the University of Wisconsin-Madison who began ALS research at a patient's behest. So the next time you're tagged to dump ice (or whatever) for the disease research du jour, go ahead. It helps.Could Copper Lead To A Cure For ALS?
After decades of frustratingly little progress, scientists recently showed that the motor-neuron breakdown accompanying ALS may be linked to a genetic mutation in a protein called copper-zinc-superoxide dismutase (SOD1).
While looking at stem cells with the mutation, Zhang found an imbalance that caused the neurofilaments to tangle, which is a cause of ALS. A paper he published in April demonstrates that the damage is reversible once the mutation is corrected.
In June, Beckman published a study suggesting that the SOD1 mutation may be associated with a cellular copper deficiency. When Beckman gave mice with the mutation an oral copper compound, it improved their ability to move and extended their lives by 12 percent, offering a promising avenue for therapeutics research.
This article was originally published in the November 2014 issue of Popular Science, under the title "Slacktivism Drives Science Forward".
The treatment, developed by researchers in the UK and Poland, involved removing one of Fidyka's olfactory bulbs (the structures in the brain that allow you to smell) growing cells from the bulb, and then injecting those cells into the damaged area of Fidyka's spinal cord. The researchers were interested in cells from the olfactory bulb in particular because the nerves in the olfactory system are the only part of the human nervous system known to regrow after being damaged, with the help of olfactory ensheathing cells.
The researchers are looking to use less invasive techniques in the future, because undergoing brain surgery to extract the olfactory tissue isn't anyone's idea of a good time, much less someone who is paralyzed.
The BBC reports that over 100 micro injections of olfactory ensheathing cells were injected into the injury site, and strips of nerve tissue from Fidyka's ankle were laid across the gap in the spinal cord, in the hopes that the cells from the olfactory bulbs would encourage regrowth. A similar procedure had been sucessfully tested on dogs in 2012.
Now, 19 months after the operation, Fidyka has regained sensation in parts of his lower body, and after intense physical therapy is able to walk using a walker. As an added bonus, even with one olfactory bulb removed, Fidyka retained his sense of smell.
He told the BBC: "I think it's realistic that one day I will become independent. What I have learned is that you must never give up but keep fighting, because some door will open in life."
The story is the subject of an episode of the BBC television program Panorama airing today at 10:35 pm in the UK. The study itself will be published in the journal Cell Transplantation at a later date, but the researchers acknowledge that as exciting as this result is, there is still a lot more work to be done.
"Our results are very encouraging," the medical team is quoted as saying in a statement. "However, our results need to be confirmed in a larger group of patients with a similar injury. In the meantime, we are investigating surgical techniques for more minimally invasive access to the olfactory bulb."
When the first working gun was 3-D printed in the United States, the government responded not through the Bureau of Alcohol, Tobacco, and Firearms, but instead through the State Department. Guns, it turns out, aren’t terribly hard to get in the United States, so a 3-D printed gun doesn’t radically change gun access here. In countries with stricter gun control laws, though, printing a gun is a new risk. This week, Japan sentenced 28-year-old Yoshitomo Imura to two years in prison for printing guns and instructing others on how to print them.
Imura printed a six-shot revolver known as the ZigZag. It fires .38 caliber bullets, same as those used in Defense Distributed’s original 3-D printed Liberator pistol. While the majority of the gun is printed plastic, it still has a few non-printed parts. Notably, these are pins, screws, a spring, and several rubber bands. Here’s a video of someone assembling a printed ZigZag revolver:
Japan isn’t the only country with tight gun control laws to address 3-D printed weapons. In Australia, which passed strong gun control measures following a 1996 massacre, police tested 3-D printed guns. Their tests highlight how likely it is for poorly-constructed guns to explode, portraying them as a major risk to the shooter as well as anyone standing in the vicinity. In October 2013, the United Kingdom launched a raid on suspected 3-D gun printers. The raid yielded only 3-D printer parts, not guns.
In the United States, 3-D printed guns are regulated by the Undetectable Firearms Act, which specifies that guns must be visible to metal detectors. Defense Distributed's Liberator included a functionless 6-ounce metal bar in the handle for just this purpose. In the United States, detectability might be more important than just the creation of new weapons, but in countries without more than 200 million guns in private hands, the mere creation of a new gun is itself a new risk.ZigZag Revolver Assembled Screenshot, "3D Printed Guns First in the world 3D Zig Zag Revolver Made in Japan"
The human subjects went on a trip from the U.S. to Israel -- an eight- to ten-hour time zone difference. The mice in the study didn't get to go anywhere (humans have all the fun), but they had their feeding habits and the light in their habitats disrupted. In both the humans and the mice, the researchers took fecal samples before and after to see which bacteria were thriving in their guts. Not only did they find that the bacteria in the gut changed, they found that the bacteria who thrived under the changing conditions were the ones most associated with obesity and other health issues.
"Our findings highlight a new therapeutic target that may be exploited in future studies to normalize the microbiota in those people whose lifestyle involves frequent alterations in sleep patterns, such as shift workers and very frequent fliers," study author Eran Elinav said in a press release. "Targeting the harmful changes in the microbiota in these large human populations with probiotic or antimicrobial therapies may reduce or even prevent their risk of developing obesity and its complications."
Jet lag and lack of sleep due to shift work are linked to health problems, including gastrointestinal, metabolic issues, and fatigue. In the study, the researchers found that the 'jet-lagged' mice gained weight compared to their non-fake-jet-setting counterparts. The humans also experienced changes to the microbiome, but luckily the effects dissipated within a few weeks.