We’re excited to share the first in a series celebrating work/life balance in the Emory University Department of Chemistry. Click the photo to read!
By Ben Yin (Hill Group)
Reposted with permission from Inscripto: The Science Writers Association of Emory. Originally published April 14th, 2015.
In the pilot episode of the iconic 80s TV show, MacGyver, the titular character made his debut as a resourceful secret agent by making a sodium bomb to take down a wall, rescuing a couple of scientists. For MacGyver, with his extensive knowledge of the physical sciences, the process was simple: he immerses pure sodium metal inside a bottle of water and the explosive reaction between sodium and water is great entertainment for viewers of all ages.
Today, this little display of pyrotechnic shenanigans is often seen in high school chemistry demos. Alternatively, one can find many dozens of internet videos documenting this violent reaction between alkali metals like sodium or potassium and water, often accompanied by exclamations and whistles of joy. It’s no surprise that some of these videos have also gone viral. This amusing diversion of chucking alkali metals into water to watch it explode has been around since the 19th century and scientists have had a solid description of the nature of this reaction for about as long. Or so we thought.
The classic explanation of elemental sodium’s volatile reaction with water involves the simple reduction-oxidation chemistry of sodium and water: electrons flow from sodium metal into the surrounding water, forming sodium hydroxide and hydrogen gas. This is a very fast reaction that produces a lot of heat. Hydrogen gas is extremely flammable in air, and in the presence of a heat source, this mixture can lead to a hydrogen explosion, not unlike the infamous incident that allegedly set the Hindenburg zeppelin aflame. The release of the large amount of energy in these reactions results in rapid expansion of the surrounding gas, which is what causes chemical explosions.
Generations of chemists have accepted this seemingly obvious explanation without much deliberation. It is perhaps surprising then, that one curious soul decided to look at this century-old reaction more in-depth.
Philip Mason earned his PhD in chemistry and has co-authored more than 30 scientific papers, but is probably better known for his YouTube channel, where he regularly posts videos, often in vlog format, under the pseudonym “Thunderf00t” (yes, that’s two zeros substituting for the letters “O”). His favorite post topics are often pieces of popular science he encounters, and Mason has earned the support of a huge public following with his YouTube channel. In 2011, using donations from some of his more than 300,000 YouTube subscribers, Mason purchased the materials and consumer grade high-speed cameras necessary to look at what he thought would be “home chemistry.”
The YouTube project, it turns out, raised many questions, for which Mason found traditional answers unsatisfactory, namely the explosive nature of alkali metals in water. Compelling footage also showed a secondary gas explosion above the water surface that resembles a hydrogen explosion, demonstrating that the initial stronger and faster explosion can’t be explained with our traditional understandings of this reaction. Some scientists have suggested, instead, that the explosion is caused by the sheer amount of heat released during the reaction. If this were the case, the heat would boil the water and a rapid generation of steam leads to explosion. Mason remained unconvinced. A key insight by Mason and his colleagues was that as hydrogen and steam are generated when the alkali metal comes into contact with water, the interface between the metal and water should be blocked off by the products and therefore inhibit further reaction. This would result in the exact opposite of the explosive reactions being observed. Crucially, immersing solid chunks of sodium and potassium under water still results in rapid explosions, so this too could not be the explanation for the initiation of the explosion. These enigmas led Mason to bring his YouTube project into the lab.
To get a better look at the reaction, Mason and his colleagues turns to research grade high-speed cameras. Filming at around 10,000 frames per second, they were able to capture the beginning of the reaction between alkali metals and water in astounding detail. What they captured is striking: the reaction is immediate, and the metal shatters on contact with the water surface. Within two-ten thousandths of a second, spikes of metal are flying apart from anywhere the surface touches water. As the sheer force of the rupturing metal bursts forth, a brilliant blue wash appears to stain the blast of water in the very next frame. This stunning blue color is due to solvated electrons in water, which is usually far too short-lived for people to see.
What isn’t so easy to interpret are the metal spikes flying apart, piercing the water in the process. However, with some chemical intuition and computing time on supercomputers, Mason and his colleagues came up with an explanation for this observation that ultimately describes the explosive nature of alkali metals in water.
When large numbers of electrons escape from the alkali metals into the surrounding water, the metal itself becomes extremely positively charged. Like the static charges that can make our hair spike up for that mad scientist look, the positive metal atoms now repel each other, except with much more violent force. Atoms that were previously bonded together as a solid now suddenly fly apart at extraordinary speed. This, in turn, exposes fresh metallic surfaces to water for the explosive reaction to take place. This little-known phenomenon is called Coulomb explosion.
The immediate application of this knowledge for preventing explosions in industrial use of alkali metals will be useful. Just as important, the discovery of this mechanism of explosion in a chemical reaction over a century old reminds us not only of how little we know, but also how much we simply fail to even consider. In the face of public apathy for science, it is encouraging that such a significant scientific discovery should come from a YouTuber, funded partially by the YouTube community, and documented in vlog format throughout the research process. It leaves us wondering what other remarkable discoveries such public engagement could lead to.
Mason and his colleagues published their research in the February issue of Nature Chemistry, they acknowledged the support of his YouTube followers.
Here’s the video: https://www.youtube.com/watch?v=LmlAYnFF_s8
Link for article: http://www.nature.com/nchem/journal/v7/n3/full/nchem.2161.html
By Kevin Sullivan (Hill Group)
Reposted with permission from InScripto: The Science Writers Association of Emory. Originally published April 8th, 2015.
There is a good chance that you personally know someone suffering from Alzheimer’s disease. This is unsurprising, as it is estimated that one out of every nine people over 65 is affected, making it the most common form of dementia. Initially, someone with Alzheimer’s will show signs of forgetfulness and disorientation which may not be immediately noticeable. A person might find themselves losing their keys more often or asking the same question multiple times in a conversation without realizing it. These symptoms gradually get worse over a period of three to nine years, leading to more severe memory loss, mental and physical impairment, and eventually resulting in death. According to the 2014 World Alzheimer Report, 44 million people are living with dementia worldwide, with the number set to double by 2030. Aside from the devastating emotional costs imposed upon the individuals and their care providers, usually family members, the economic impact of dementia is an imposing figure. In 2010, the cost of care for dementia was $604 billion, with costs expected to exceed $1 trillion by 2030.
Decades of research have revealed several risk factors for the disease, such as age, head trauma, heart disease, and sex (women may be more susceptible than men). Despite information about these risk factors and studies revealing the differences between the brains of people with Alzheimer’s relative to those of healthy people, the exact cause still remains a mystery. In recent years, researchers have discovered many clues that have gotten us closer to solving this mystery. One of the key findings is that the degeneration of the brain in Alzheimer’s is associated with the presence of protein fragments called amyloid beta peptides. Amyloid beta is present in healthy brains as well, but problems arise in Alzheimer’s when these peptides become folded in an incorrect way, causing them to associate with one another and form clumps, called plaques, which deposit in the brain.
Another major finding is that tau proteins, which normally help to stabilize the structural components of cells, can become defective in Alzheimer’s disease, causing them to get tangled up and deposit in the brain. Both amyloid beta plaques and tau protein tangles are quite toxic to nerve cells and eventually result in the death of the neurons that make up the brain. Despite these and a variety of other clues that have been discovered, Alzheimer’s is plagued by the classic chicken-or-egg question: which of the observed problems are causes of the disease, and which ones are a result of the disease process? So far, this question has been very difficult to answer. Only one form of Alzheimer’s, known as early onset familial Alzheimer’s disease, has a definite cause involving a mutation in specific genes that produce amyloid beta proteins. However, these mutations are the cause of only 1 to 5 percent of cases, while the origin of the rest of the cases remains unclear.
The field of Alzheimer’s research is rapidly advancing, with new discoveries made nearly every day. One intriguing recent discovery suggests that an immune response may be responsible for the progression of Alzheimer’s disease. In a March 2015 review published in Nature Immunology, a group led by Michael T. Heneka from the University of Bonn explained some of these recent findings. One of these hypotheses proposed explains that, because amyloid beta is found in several different viruses and bacteria, the body developed an immune system response to the peptide in order to fight off these pathogens. In some cases, the immune response can become misdirected and targets the amyloid beta found in human tissue instead of that of an invader, which is known as an autoimmune response. When the immune system attacks tissue within the brain, it causes damage to the local neurons and leads to destruction of brain tissue.
The immune response in the brain is controlled by cells called microglia. These cells act as the guard dogs of the central nervous system, both defending against infections and scavenging damaged cells and waste found around the brain. Much like certain dogs, they can have extremely strong reactions to even small disturbances. This sensitivity, while quite advantageous for quickly responding to threats, can also have major consequences if they become so sensitive that they start attacking human tissues. Once the microglia are activated, they release molecules that trigger inflammation in surrounding tissue. Inflammation is a process that normally helps to eliminate the initial cause of an injury and help with tissue repair, but persistent inflammation will result in significant cellular damage. Moreover, this response actually makes it more difficult for the body to clear beta amyloid plaques, causing a negative feedback loop that results in even more plaque deposition in the brain.Adding more evidence to this theory, a new study published in the Journal of Alzheimer’s Disease on February 2015 by the Bieberich lab at Georgia Regents University demonstrated that an autoimmune response might be responsible for the progression of the disease. Researchers have discovered that a molecule called ceramide, mainly found in membranes surrounding cells throughout the body, can be targeted by the immune system. This immune response causes an increase in antibodies that destroy ceramide in the brain. The researchers found that when amyloid beta plaques start to build up in the brain, certain cells begin producing more ceramide. The ceramide is then targeted by the immune system, causing inflammation and increasing the amount of amyloid beta in the brain. These new studies suggest that our own immune response, then, may be what is ultimately responsible for the advancement of the disease.
While we may still not know the root cause behind the mystery of Alzheimer’s disease, these new findings have revealed another important clue, which is that autoimmune responses may play a significant role in the progression of the disease. One of the exciting aspects of this research is that it opens up a whole new set of opportunities to treat Alzheimer’s using therapeutics that target the microglia or reduce inflammation in the brain, which may be able to slow down the progression of the disease. More effective treatments are sure to significantly address the mounting healthcare costs associated with the growing population afflicted with this disease. More importantly, these new treatments have the potential to provide life-altering relief to those currently suffering from Alzheimer’s.