Sparkonit delivers information on latest discoveries and hottest trailblazing researches together with short, entertaining and inspiring science videos. Its mission is to spread scientific knowledge in an easy and extensive way that does not bore its readers and inspire them with what science can do.
Stephen Hawking, one of the greatest theoretical physicists, has died at his home in Cambridge. He was 76.
At the age of 21, Hawking was diagnosed with amyotrophic lateral sclerosis (ALS), a rare neurodegenerative disease commonly known as Lou Gehrig’s Disease. It left him wheelchair-bound and totally paralyzed.
ALS normally claims the lives of those affected within three to five years after diagnosis, but Hawking managed to survive for more than half a century.
In 1974, Hawking stunned the world by showing that blackholes emit a radiation known as Hawking Radiation. According to Hawking Radiation, blackholes “create and emit sub-atomic particles until they exhaust their energy and evaporate completely.”
He also showed the world the connection between blackholes, physics and thermodynamics, and that has been a central theme theoretical physics ever since. Hawking also authored and co-wrote numerous books, including “A Brief History Of Time”.
RIP Stephen Hawking (January 8, 1942 – March 14, 2018)
Researchers at Yale University in New Haven, CT, have discovered that intestinal bacteria in mice and humans can travel to other organs and evoke autoimmune response. But, administering antibiotic or vaccine that targets the bacteria can subdue this autoimmune reaction.
In autoimmune diseases, our immune system which is supposed to protect us turns on us and starts attacking our healthy cells and tissues. As a result, our body’s ability to fight off foreign invaders decreases, making us susceptible to range of infections. Some of the most common autoimmune diseases are rheumatoid arthritis, inflammatory bowel disease (IBD), psoriasis and type 1 diabetes.
Scientists have not fully understood the cause of autoimmune diseases, but they have long suspected bacteria in the gut to be the culprit as a variety of autoimmune conditions have been linked to it.
In the study, senior author Martin Kriegel, M.D. and his team centered on a gut bacteria called Enterococcus gallinarum, which can “translocate” to lymph nodes, the liver, and spleen. Using a genetically susceptible mouse model, they were able to observe that once traveled beyond the gut, E. gallinarum triggered autoimmune responses and initiated producing auto-antibodies and inflammation.
Researchers were able to substantiate the same mechanism of inflammation in cultured liver cells of healthy people. They also found E. gallinarum to be present in livers of patients with autoimmune disease.
Further experiments showed that autoimmunity in the mice can be suppressed with an antibiotic or a vaccine designed to target E. Gallinarum. Either of the approach inhibited the growth of the bacterium in the tissues and alleviated its effects on the immune system.
“When we blocked the pathway leading to inflammation, we could reverse the effect of this bug on autoimmunity,” Martin Kriegel, M.D. explained. “The vaccine against E. gallinarum was a specific approach, as vaccinations against other bacteria we investigated did not prevent mortality and autoimmunity.”
The findings were published in the journal Science. Researchers believe treatment of chronic autoimmune conditions, including systemic lupus and autoimmune liver disease, can be made easy with further research on E. gallinarum and its mechanisms.
A gene is a segment of DNA that contains a set of instructions to make molecules that organisms need to survive. In a process called gene expression, these instructions are converted into some sort of product. And the product usually is either a protein or functional RNA.
So what is gene expression? And, how do genes express themselves? To understand them, it’s crucial that you know the process called protein synthesis because gene expression and protein synthesis are basically the same molecular process. And being familiar with these processes will help you better understand the underlying causes of cancer, and eventually help you find better diagnosis and treatment for the same.
Proteins make up the enzymes and other essentials elements cells need to survive and to keep the body healthy. All proteins are made of chains of amino acids. Cells make their proteins using the information stored in their genes in a process called protein synthesis. In their DNA each gene carries the information in the sequence of bases that make up the gene. Now, let’s explore the relationship between DNA, chromosomes and genes.
Each long molecule of DNA, each chromosome is divided into genes. And each gene contains the instruction the cell requires to make a protein. The instruction tells which amino acids are needed to make that protein and in what order to put them. This information is spelled out in the sequence of cross pieces that make up the DNA in that gene.
The cross pieces are made up of pairs of chemical units called bases, which are abbreviated A, C, G and T. The bases pair up only one way – A pairs with T and C pairs with G, this is called complementary base pairing. The information in DNA (the message encoded in that gene) is spelled out in the sequence of those A’s, C’s, G’s and T’s along the length of the gene.
During protein synthesis, the sequence of bases in a gene’s DNA is copied, then the copy is used to make a protein. The process happens in four steps: gene activation, gene transcription (copying the DNA message in the gene), gene editing (editing the message), and translation (translating the message into a protein).
Gene Activation – it happens when a protein called a transcription factor binds with the gene at a certain place on the gene.
Gene Transcription – the DNA for the activated gene unwinds and opens up during this stage. This exposes the sequence of A’s C’s GS and T’s and the genes DNA. The sequence of bases is copied in the form of RNA. Like DNA, RNA is made up of bases but RNA has only one strand rather than two as in DNA . Also RNA does not use the base abbreviated “T” (thymine) – instead it has a base call to uracil abbreviated “U”. So as the RNA copy is made, every A in the DNA is copied as U in the RNA. This RNA is called messenger RNA (or, mRNA)
Editing – the mRNA is edited. Unneeded bits of it are cut out and removed. The remaining mature messenger RNA molecule then leaves the nucleus and enters the cell cytoplasm.
Translation – As mRNA enters the cytoplasm, the information encoded in it is read by small structures called ribosomes. The ribosomes move along the strand of messenger RNA reading the sequence of bases and as they do, they ate amino acids one by one to a growing, chain rule that will become the final protein.
But, what does protein synthesis have to do with cancer?
The protein produced by a gene and the RNA copy of the gene are called the products of the gene. In fact, the term gene products is a general name for the RNA and protein made by activated genes during the process.
Gene expression is one more important term that relates protein synthesis to cancer. Like I mentioned above, it’s basically the same molecular process as protein synthesis, and it refers to how busy or how active a gene is in making its products. In healthy cells, which genes express themselves, how much they express themselves and when they express themselves are carefully balanced and highly controlled.
Cancer happens because cells grow out of control and that happens because some genes express themselves too much, others express themselves too little or not at all, or they express themselves at the wrong time.
You certainly don’t want to miss this. Watch Morgan Freeman, Brian Cox, Carl Sagan and Sir David Attenborough calmly explaining our universe’s beautiful journey since the Big Bang in this stunning 10 minute timelapse video.
Engineers at University of Tokyo have created tiny lights that can levitate using ultrasonic waves. Named Luciola for its resemblance to the firefly, the particle weighs 16.2 mg, has a diameter of 3.5 mm, and glows red – bright enough to illuminate text.
“Ultimately, my hope is that such tiny objects will have smartphone capabilities and be built to float about helping us in our everyday lives in smarter ways,” Makoto Takamiya, circuit design specialist who has been working on Luciola for two years, told Reuters.
Luciola emits ultrasonic waves that make it float through 285 microspeakers, and they all operate at a frequency inaudible to the human ear, allowing Luciola to levitate in total silence. In the future, the developers aspire to equip Luciola with movement or temperature sensors, which would allow the lights to deliver a message, make moving displays, detect the presence of humans and even participate in projection mapping.
Takamiya hopes to make Luciola available in the market in the next five to 10 years.
Without salt, your favorite foods such as french fries, potato chips, and chocolate chip cookies would all taste bland. And that’s because salt has lots of effects on flavor perception than just making things more salty.
Many say a spoonful of sugar helps the medicine go down, but a pinch of salt, in fact, does the work better. How is that? And why does salt make food taste better? Hank Green from SciShow explains.
Our brains are hardwired to crave salt because we need it to survive. Salt – usually sodium in the form of sodium chloride— is an essential nutrient, and our body uses it for everything from regulating fluids, blood pressure and to creating nerve impulses. But, our body can’t make sodium by itself, so we have to get at least some of it from our diet.
Humans mostly taste saltiness, thanks to epithelial sodium channels (eNaC), which are basically pores that allow sodium ions to pass into the taste receptors cells (TRCs) in the taste buds. TRCs then tell the brain that something’s salty.
Salt also suppresses bitterness better than sugar. Researchers haven’t completely figured out the mechanism for it, but study suggests it involves both the tongue and the brain. Most of the bitterness-blocking happens in the taste buds, and what researchers think sodium does here is that it interferes with the binding between bitter compounds and their taste cell receptors.
“If you’re given salt and a bitter compound in such a way that they don’t mingle on your tongue, you still perceive the overall flavor as slightly less bitter” Hank explains in the video. “That suggests some of the anti-bitterness effect comes from how your brain interprets multiple taste signals when they include saltiness.”
Salt also makes food taste better by making them smell better. The ions in the salt are attracted to some of the available water in the food. So adding salt to foods makes it easier for volatile compounds — molecules that evaporate quickly and often contribute to aroma of the food — to escape into the air. These compounds may not hit our tongue, but they are important in our perception of flavor.
“Salt also seems to do other things to make food more enjoyable … although scientists can’t really explain them yet,” says Hank. “For instance, volunteers in a 1985 study said salted split pea soup was not only saltier, sweeter and less bitter than the unsalted version — it was also thicker and fuller, altering what food scientists call mouthfeel.”
After all, saltiness is one of the fundamental flavors of human taste – maybe this also partially explains why it enhances flavor. Other tastes human tongue can detect are: bitter, sweet, sour, and umami (savory taste).
Light is made of individual photons, and these particles do not usually interact with each other. But a team of physicists from MIT and Harvard have successfully made three photons interact to form a completely new kind of photonic matter, in a breakthrough that could open a path toward using photons in quantum computing.
Professor Vladan Vuletic of MIT and Mikhail Lukin of Harvard University lead the MIT-Harvard Center for Ultracold Atoms, and together they have spent years looking for ways to make photons interact with each other. Their first success came in 2013 when they observed pairs of photon photons interacting and binding together, creating an entirely new state of matter – but they weren’t sure if interactions could take place between not only two photons, but more.
“You can combine oxygen molecules to form O2 and O3 (ozone), but not O4, and for some molecules you can’t form even a three-particle molecule,” says Vuletic in a news release. “So it was an open question: Can you add more photons to a molecule to make bigger and bigger things?”
To find out, the team created the same experimental set up they used to observe two photons interactions. The experiments involved shining a very weak laser beam through the cloud of rubidium atoms chilled to a millionth of a degree above absolute zero. The reason they cooled rubidium atoms was to slow them down or stop them. Their next step was to shine a very weak laser beam through this cloud of supercooled atoms, so that they could measure few of the photons that managed to travel through the cloud.
Normally, photons have no mass, and they travel at the speed of light – 300,000 kilometers per second. But researchers found that the photons that came out off the other side of the cloud were strongly bound together with each other and they streamed out as pairs and triplets as “single photons.” And what’s more? The bound photons had actually acquired a fraction of the mass of an electron, and moved 100,000 times slower than the normal photon.
The experiment did not end there.
The team also developed a hypothesis to explain what caused the photons to interact in the first place. Their model suggests that as a single photon moves through the cloud of rubidium atoms, it basically lands on an atom that’s at close quarter and then jumps on to the next.
Another photon travelling through the cloud also briefly binds to a rubidium atom, forming a polariton — a hybrid that is part photon, part atom. If multiple polaritons formed in the cloud, they interact with other by the way of their atomic components. And when they reach the edge of the cloud, the rubidium atoms stay behind, while the photons exit, still bound together.
The same phenomenon occurs with three photons – and they form an even stronger bond than when they make two photons interact.
“What was interesting was that these triplets formed at all,” Vuletic says. “It was also not known whether they would be equally, less, or more strongly bound compared with photon pairs.”
The entire interaction process occurs within a millionth of a second, and researchers say photons that have interacted with each other can be considered as “entangled,” which is a key property for any quantum computing bit.
“Photons can travel very fast over long distances, and people have been using light to transmit information, such as in optical fibers,” Vuletic says. “If photons can influence one another, then if you can entangle these photons, and we’ve done that, you can use them to distribute quantum information in an interesting and useful way.”
Going forward, the team aims to figure out ways to coerce other interactions among photons, such as repulsion – where photons scatter off each other.
“It’s completely novel in the sense that we don’t even know sometimes qualitatively what to expect,” explains Vuletic. “With repulsion of photons, can they be such that they form a regular pattern, like a crystal of light? Or will something else happen? It’s very uncharted territory.”
Researchers at University of Colorado Boulder have developed an electronic skin that can heal itself – and is also fully recyclable. According to the paper published in the journal Science Advances, the e-skin is a thin, translucent material with sensors embedded to mimic function and mechanical properties of human skin such as sensing pressure temperature, humidity and air flow.
The uniqueness about this piece of technology is that it’s made of a polymer called polyimine (made of three commercially available compounds – terephthalaldehyde, diethylenetriamine, and tris(2-aminoethyl)amine – mixed together in ethanol) laced with silver nanoparticles to withstand stress, conduct electricity and provide chemical stability. And what’s more? When the skin is cut in two, polyimine can recreate chemical bonds between two sides – allowing the e-skin to heal itself completely.
“What is unique here is that the chemical bonding of polyimine we use allows the e-skin to be both self-healing and fully recyclable at room temperature,” said Jianliang Xiao, an assistant professor in CU Boulder’s Department of Mechanical Engineering in a news release. “Given the millions of tons of electronic waste generated worldwide every year, the recyclability of our e-skin makes good economic and environmental sense.”
Another cool feature about this e-skin is that you can make it wrap around curve surfaces like human arms and robotic hands by using a modest amount of heat and pressure.
“Let’s say you wanted a robot to take care of a baby,” said Zhang. “In that case you would integrate e-skin on the robot fingers that can feel the pressure of the baby. The idea is to try and mimic biological skin with e-skin that has desired functions.”
“This particular device … won’t produce any waste,” Xiao told the Verge. “We want to make electronics to be environmentally friendly.”
So if the e-skin is damaged beyond repair, it is soaked into ‘recycling solution’. This solution degrades polymers into smaller molecules that are soluble in ethanol, allowing the silver nanoparticles fall to the bottom of the solution. The left-over materials is then re-used to make another fully functioning e-skin.
Researchers say e-skin could have potential applications in making of prosthetics, robots, or smart textiles – all without having to worry about producing more e-waste. However, Xiao says the e-skin is yet to be perfected, because it’s not as stretchy as human skin. Right now, he and his team are working to improve the device’s scalability.
Neuroscientists at University of California have identified ‘anxiety cells’ in the brain’s hippocampus. The finding, so far demonstrated with mice, could lead to better treatments for anxiety disorders in humans because the cells probably exist in humans, too, researchers say.
“Now that we’ve found these cells in the hippocampus, it opens up new areas for exploring treatment ideas that we didn’t know existed before,” said the study’s lead author, Jessica Jimenez, in a news release.
For the study, researchers inserted miniature microscope into the brains of the mice to record the activity of hundreds of cells in the hippocampus as the mice moved through their surroundings. They found that whenever the mice were exposed to anxiety-provoking environments, cells in the ventral part of the hippocampus were active. And when the researchers traced the output of those cells, it pointed to the hypothalamus – a part of the brain known to control behaviour associated with anxiety in humans.
Researchers were able to control the activity of anxiety cells, too, using a technique called optogenetics, which uses beams of light to turn the cells off and on.
The study, entitled “Anxiety Cells in a Hippocampal-Hypothalamic Circuit” has been published in the journal Neuron.
Researchers at Virginia Tech have found that mosquitoes can rapidly learn and remember the smells of hosts. Individuals deemed delicious-smelling might find themselves under siege from the mosquitoes, but if that individuals swat at them or perform other defensive behaviours – their preference can shift.
“Unfortunately, there is no way of knowing exactly what attracts a mosquito to a particular human — individuals are made up of unique molecular cocktails that include combinations of more than 400 chemicals,” Chloé Lahondère, a research assistant professor in the Department of Biochemistry said in a news release. “However, we now know that mosquitoes are able to learn odors emitted by their host and avoid those that were more defensive.”
In the study, the team demonstrated that mosquitoes exhibit a trait known as aversive learning by training female Aedes aegypti mosquitoes to associate odors (including human body odors) with unpleasant shocks and vibrations.
When the team assessed the same mosquitoes 24 hour later in a Y-maze olfactometer where they had to fly upwind and choose between the once-preferred human body odor and a control odor, the bugs avoided the human body odour – suggesting that they had been successfully trained to identify human by odors and associate those smells with an unpleasant sensation. The team also found that dopamine is critical for aversive learning in mosquitoes. Manipulating the dopamine receptor prevents mosquitoes from learning the smells of hosts.
“Understanding these mechanisms of mosquito learning and preferences may provide new tools for mosquito control,” said Clément Vinauger, an assistant professor of biochemistry in Virginia Tech’s College of Agriculture and Life Sciences. “For example, we could target mosquitoes’ ability to learn and either impair it or exploit it to our advantage.”
The study, entitled “Modulation of Host Learning in Aedes aegypti Mosquitoes” has been published in the journal Current Biology