What makes fireworks colorful?
It’s all thanks to the luminescence of metals. When certain metals are heated (over a flame or in a hot explosion) their electrons jump up to a higher energy state. When those electrons fall back down, they emit specific frequencies of light - and each chemical has a unique emission spectrum.
You can see that the most prominent bands in the spectra above match the firework colors. The colors often burn brighter with the addition of an electron donor like Chlorine (Cl).
But the metals alone wouldn’t look like much. They need to be excited. Black powder (mostly nitrates like KNO3) provides oxygen for the rapid reduction of charcoal © to create a lot hot expanding gas - the BOOM. That, in turn, provides the energy for luminescence - the AWWWW.
Aluminium has a special role — it emits a bright white light … and makes sparks!
Images: Charles D. Winters, Andrew Lambert Photography / Science Source, iStockphoto, Epic Fireworks, Softyx, Mark Schellhase, Walkerma, Firetwister, Rob Lavinsky, iRocks.com, Søren Wedel Nielsen
How the Geneva Drive (the mechanical step that makes the second hand on a clock work by turning constant rotation into intermittent motion) works.
There are interesting asteroid characters in our solar system, including an asteroid that has its own moon and even one that is shaped like a dog bone! Our OSIRIS-REx mission launches at 7:05 p.m. EDT today and will travel to asteroid Bennu.
Scientists chose Bennu as the target of the OSIRIS-REx mission because of its composition, size and proximity to Earth. Bennu is a rare B-type asteroid (primitive and carbon-rich), which is expected to have organic compounds and water-bearing minerals like clays.
Our OSIRIS-REx mission will travel to Bennu and bring a small sample back to Earth for study.
When talking about asteroids, there are some terms scientists use that might not be in your typical vocabulary…but we’ll help with that!
Orbital Eccentricity: This number describes the shape of an asteroid’s orbit by how elliptical it is. For asteroids in orbit around the sun, eccentricity is a number between 0 and 1, with 0 being a perfectly circular orbit and 0.99 being a highly elliptical orbit.
Inclination: The angle, in degrees, of how tilted an asteroid’s orbit is compared to another plane of reference, usually the plane of the Earth’s orbit around the sun.
Orbital Period: The number of days it takes for an asteroid to revolve once around the sun. For example, the Earth’s orbital period is 365 days.
Perihelion Distance: The distance between an asteroid and the sun when the asteroid is closest to the sun.
Aphelion Distance: The distance between the asteroid and the sun when the asteroid is farthest away from the sun.
Astronomical unit: A distance unit commonly used to describe orbits of objects around the sun. The distance from the Earth to the sun is one astronomical unit, or 1 AU, equivalent to about 93 million miles or 150 million kilometers.
Diameter: A measure of the size of an asteroid. It is the length of a line from a point on the surface, through the center of the asteroid, extending out to the opposite surface. Irregularly shaped asteroids may have different diameters depending on which direction they are measured.
Rotation Period: The time it takes for an asteroid to complete one revolution around its axis of rotation. For example, the rotation period of the Earth is approximately 24 hours, or 1 day.
Spectral Type: The classification of an asteroid, based on a measurement of the light reflected by the asteroid.
Watch live launch coverage of OSIRIS-REx to asteroid Bennu starting at 5:30 p.m, on NASA TV: http://www.nasa.gov/nasatv
Make sure to follow us on Tumblr for your regular dose of space: http://nasa.tumblr.com
English-speaking parents tend to use vague, one-size-fits-all verbs as they emphasize nouns: cars, trucks, buses, bicycles and scooters all simply “go.” Mandarin speakers do the opposite: they use catchall nouns such as “vehicle” but describe action—driving, riding, sitting on, pushing—with very specific verbs. “As a native English speaker, my first instinct when a baby points is to label,” Tardif says. Her babysitter, on the other hand, was a native Mandarin speaker, whose instinct was to name the action she thought the child was trying to achieve.
via Twitter
Chronic stress can lead to changes in neural circuitry that leave the brain trapped in states of anxiety and depression. But even under repeated stress, brief opportunities for recovery can open up, according to new research at The Rockefeller University.
(Image caption: Routine versus disruptive: A familiar stressor (left) did not increase NMDA receptors (dark spots), a booster of potentially harmful glutamate signaling, in the brains of mice. However, when subjected to an unfamiliar stress (right), mice expressed more NMDA receptors)
“Even after a long period of chronic stress, the brain retains the ability to change and adapt. In experiments with mice, we discovered the mechanism that alters expression of key glutamate-controlling genes to make windows of stress-related neuroplasticity—and potential recovery—possible,” says senior author Bruce McEwen, Alfred E. Mirsky Professor, and head of the Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology. Glutamate is a chemical signal implicated in stress-related disorders, including depression.
“This sensitive window could provide an opportunity for treatment, when the brain is most responsive to efforts to restore neural circuitry in the affected areas,” he adds.
The team, including McEwen and first author Carla Nasca, wanted to know how a history of stress could alter the brain’s response to further stress. To find out, they accustomed mice to a daily experience they dislike, confinement in a small space for a short period. On the 22nd day, they introduced some of those mice to a new stressor; others received the now-familiar confinement.
Then, the researchers tested both groups for anxiety- or depression-like behaviors. A telling split emerged: Mice tested shortly after the receiving the familiar stressor showed fewer of those behaviors; meanwhile those given the unfamiliar stressor, displayed more. The difference was transitory, however; by 24 hours after the final stressor, the behavioral improvements seen in half of the mice had disappeared.
Molecular analyses revealed a parallel fluctuation in a part of the hippocampus, a brain region involved in the stress response. A key molecule, mGlu2, which tamps down the release of the neurotransmitter glutamate, increased temporarily in mice subjected to the familiar confinement stress. Meanwhile, a molecular glutamate booster, NMDA, increased in other mice that experienced the unfamiliar stressor. In stress-related disorders, excessive glutamate causes harmful structural changes in the brain.
The researchers also identified the molecule regulating the regulator, an enzyme called P300. By adding chemical groups to proteins known as histones, which give support and structure to DNA, P300 increases expression of mGlu2, they found.
In other experiments, they looked at mice genetically engineered to carry a genetic variant associated with development of depression and other stress-related disorders in humans, and present in 33 percent of the population.
“Here again, in experiments relevant to humans, we saw the same window of plasticity, with the same up-then-down fluctuations in mGlu2 and P300 in the hippocampus,” Nasca says. “This result suggests we can take advantage of these windows of plasticity through treatments, including the next generation of drugs, such as acetyl carnitine, that target mGlu2—not to ‘roll back the clock’ but rather to change the trajectory of such brain plasticity toward more positive directions.”
A UT Dallas scientist has found a new neurological mechanism that appears to contribute to a reduction in pain.
According to Dr. Ted Price, associate professor in the School of Behavioral and Brain Sciences, the discovery of neuroligin-2 as a cause exacerbating chronic pain is significant for the research community. Although the findings likely won’t immediately lead to new pain therapies, the findings offer a potential new therapeutic direction to investigate, he said.
Price’s research on the topic has recently been published online in Pain, the journal of the International Association for the Study of Pain.
The study focused on the body’s inhibitory networks — a series of biochemical reactions that decrease certain neurological activity, such as pain. Price said a great deal of previous research in this area has focused on the activity of the neurotransmitter GABA, a chemical released by nerve cells in the brain.
Normally, a GABA neurotransmitter acts to inhibit neuronal activity, such as pain. However, when pain becomes chronic there is strong evidence that a process called GABAergic plasticity can cause GABA to lose its inhibitory activity, sometimes making the pain even worse.
The source of these excitatory actions in neuronal circuits has been broadly attributed to chloride ions, but Price’s research has found another potential cause of GABAergic plasticity: synaptic adhesion molecules called neuroligin-2.
“From a basic science perspective, we’re really excited about it because it demonstrates that the types of GABAergic plasticity that can occur in the setting of chronic pain are more diverse than we’ve appreciated before,” he said.
Price, who heads the undergraduate research program in neuroscience in the school, focuses much of his research on understanding the neuroscience behind pain, particularly chronic pain. He said individuals with chronic pain typically don’t receive the pain-reduction benefits delivered by inhibitory systems. Instead, they often experience increased pain.
“When you hit your hand with a hammer, almost everybody has the same reflex reaction — that is, to rub your finger which, in turn, helps to reduce pain. The reason that works is because it increases GABAergic inhibition in the spinal cord,” Price said. “However, people who have chronic pain — if they do the same thing — find that rubbing it actually makes the pain worse. That’s because the GABAergic system loses its efficacy and, in fact, can become excitatory.”
Price said the research is another step in determining why the GABAergic system stops working correctly in some people and provides a second theory for what drives the system.
“Having two ideas and different models will allow us to determine what the therapeutic opportunities are — creating something that will change that back to normal. The lack of performance in the inhibitory system is very detrimental to those who are in chronic pain,” he said.
Price said the development of chronic pain is, in essence, one’s body “learning” something that is bad.
“It’s changing the way the body functions — it’s learning. That learning, in the case of chronic pain, is aberrant — it’s causing the situation to get worse. If we can figure out what that form of learning was, then we can potentially reverse it. Understanding that the GABAergic system changes during this form of learning potentially offers a new therapeutic avenue,” he said.
How Printing a 3-D Skull Helped Save a Real One
What started as a stuffy-nose and mild cold symptoms for 15-year-old Parker Turchan led to a far more serious diagnosis: a rare type of tumor in his nose and sinuses that extended through his skull near his brain.
“He had always been a healthy kid, so we never imagined he had a tumor,” says Parker’s father, Karl. “We didn’t even know you could get a tumor in the back of your nose.”
The Portage, Michigan, high school sophomore was referred to the University of Michigan’s C.S. Mott Children’s Hospital, where doctors determined the tumor extended so deep that it was beyond what regular endoscopy could see.
The team members needed to get the best representation of the tumor’s extent to ensure that their surgical approach could successfully remove the entire mass
“Parker had an uncommon, large, high-stage tumor in a very challenging area,” says Mott pediatric head and neck surgeon David Zopf, M.D. “The tumor’s location and size had me question whether a minimally invasive approach would allow us to remove the tumor completely.”
To help answer that question, teams at Mott sought an innovative approach: crafting a 3-D replica of Parker’s skull.
The model, made of polylactic acid, helped simulate the coming operation on Parker by giving U-M surgeons “an exact replica of his craniofacial anatomy and a way to essentially touch the ‘tumor’ with our hands ahead of time,” Zopf says.
Just as important, it also allowed the team to counsel Parker and his family by offering them a look at what lurked within — and, with the test run successfully complete, what would lie ahead.
A ‘pretty impressive’ model
The rare and aggressive tumor in Parker’s nose is known as juvenile nasopharyngeal angiofibroma, a mass that grows in the back of the nasal cavity and predominantly affects young male teens. Mott sees a handful of cases each year.
In Parker’s case, the tumor had two large parts: one roughly the size of an egg and the other the size of a kiwi. The mass sat right in the center of the craniofacial skeleton below the brain and next to the nerves that control eye movement and vision.
“We were obviously concerned about the risks involved in this kind of procedure, which we knew could lead to a lot of blood loss and was sensitive because it was so close to the nerves in his face,” says Karl, who praised the 3-D methodology used to aid his son. “It was pretty impressive to see the model of Parker’s skull ahead of the surgery. We had no idea this was even possible.”
Zopf, working with Erin McKean, M.D., a U-M skull base surgeon, was able to completely remove the large tumor. Kyle VanKoevering, M.D., and Sajad Arabnejad, Ph.D., aided in model preparation.
Through preoperative embolization, the blood supply to the tumor was blocked off the day before surgery to decrease blood loss. A large portion of the tumor was then detached endoscopically and removed through the mouth. The remaining mass under the brain was taken out through the nose.
Doctors took pictures of Parker’s anatomy during the surgery and, later, compared it with pictures from the model. They were nearly identical.
“Words alone can’t express how thankful we are for Parker’s talented team of surgeons at Mott,” says his mother, Heidi. “Parker is back to his old self again.”
Powerful potential
Although medical application of the technology continues to gain attention, it isn’t entirely new. Zopf and Mott teams have used 3-D printing for almost five years.
Groundbreaking 3-D printed splints made at U-M have helped save the lives of babies with severe tracheobronchomalacia, which causes the windpipe to periodically collapse and prevents normal breathing. Mott has also used 3-D printing on a fetus to plan for a potentially complicated birth.
“We are finding more and more uses for 3-D printing in medicine,” Zopf says. “It is proving to be a powerful tool that will allow for enhanced patient care.”
Based on success in patients such as Parker and continued collaboration, it’s a concept that appears poised to thrive.
“Because of the team approach we’ve established at the University of Michigan between otolaryngology and biomedical engineering, the printed models can be designed and rapidly produced at a very low cost,” Zopf says. “Michigan is one of only a few places in the nation and world that has the capacity to do this.”