Why Is Machine Learning (CS 229) The Most Popular Course At Stanford? It turns out that artificial intelligence (AI) and the robotics that is tied to it, consists of two primary systems, control and perception.
Via Ben van Lier
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Most robotic parts used today are rigid, have a limited range of motion and don’t really look lifelike. Inspired by both nature and biology, a scientist from Florida Atlantic University has designed a novel robotic finger that looks and feels like the real thing. In an article recently published in the journal Bioinspiration & Biomimetics, Erik Engeberg, Ph.D., assistant professor in the Department of Ocean and Mechanical Engineering within the College of Engineering and Computer Science at FAU, describes how he has developed and tested this robotic finger using shape memory alloy (SMA), a 3D CAD model of a human finger, a 3D printer, and a unique thermal training technique.
“We have been able to thermo-mechanically train our robotic finger to mimic the motions of a human finger like flexion and extension,” said Engeberg. “Because of its light weight, dexterity and strength, our robotic design offers tremendous advantages over traditional mechanisms, and could ultimately be adapted for use as a prosthetic device, such as on a prosthetic hand.”
In the study, Engeberg and his team used a resistive heating process called “Joule” heating that involves the passage of electric currents through a conductor that releases heat. Using a 3D CAD model of a human finger, which they downloaded from a website, they were able to create a solid model of the finger. With a 3D printer, they created the inner and outer molds that housed a flexor and extensor actuator and a position sensor. The extensor actuator takes a straight shape when it’s heated, whereas the flexor actuator takes a curved shape when heated. They used SMA plates and a multi-stage casting process to assemble the finger. An electrical chassis was designed to allow electric currents to flow through each SMA actuator. Its U-shaped design directed the electric current to flow the SMAs to an electric power source at the base of the finger.
This new technology used both a heating and then a cooling process to operate the robotic finger. As the actuator cooled, the material relaxed slightly. Results from the study showed a more rapid flexing and extending motion of the finger as well as its ability to recover its trained shape more accurately and more completely, confirming the biomechanical basis of its trained shape.
The research group Quantum Technologies for Information Science (QUTIS) of the UPV/EHU-University of the Basque Country, led by the Ikerbasque professor Enrique Solano, in collaboration with an experimental group of the University of Tsinghua (Beijing, China) led by professor Kihwan Kim, has created a quantum simulator that is capable of creating unphysical phenomena in the atomic world, in other words, impossible physical phenomena. The researchers in the two groups have succeeded in getting a trapped atom to imitate behaviours that contradict its own fundamental laws, thus taking elements of science fiction to the microscopic world. "We have managed to get an atom to act as if it were infringing the nature of atomic systems, in other words, quantum physics and the theory of relativity. It is just like what happens in the theatre or in science fiction films in which the actors appear to display absurd behaviors that go against natural laws; in this case, the atoms are obliged to simulate absurd actions as if an actor in the theatre or in science fiction were involved," explained Prof Solano.
The results of this research have been published in the prestigious journal Nature Communications, in the article "Time reversal and charge conjugation in an embedding quantum simulator". The research team of the UPV/EHU's QUTIS group has been led by Prof Enrique Solano and has had the participation of Dr Lucas Lamata and Dr Jorge Casanova, currently at the University of Ulm, Germany.
In this experiment the researchers reproduced in the lab the theoretical proposal previously included in a previous piece of research led by the QUTIS group; it describes the possibility that a trapped atom can display behavior that is incompatible with the fundamental laws of quantum physics. More specifically, we are talking about operations prohibited in microscopic physical systems, such as charge conjugation, which transforms a particle into an antiparticle, or time reversal, that reverses the direction of the time arrow.
To conduct the experiment it was necessary to use a charged atom trapped by means of electromagnetic fields under the action of an advanced laser system. We could describe symmetry operations of this type as prohibited ones, as they could only exist in a universe that is different from the one we know and governed by different laws. Yet in this experiment it has been possible to simulate the realization of this set of impossible laws in an atomic system.
The UPV/EHU's QUTIS group is a world leader in quantum simulation and its influential theoretical proposals are often verified in the most advanced quantum technology laboratories. In this case, physical operations that are prohibited for the atomic world can be reproduced just as in science fiction, in other words, just as if they were taking place artificially in a quantum theater.
Can the passage of time be measured precisely, always and everywhere? The answer will upset many watchmakers. A team of physicists from the universities of Warsaw and Nottingham have just shown that when we are dealing with very large accelerations, no clock will actually be able to show the real passage of time, known as "proper time."
That might change, though, for much higher accelerations.
Anyone with a child in school is probably aware of the need for peanut free zones. You get a notice when your child returns from school on the first day stating that at least one child in their class has a peanut allergy, which means nothing with peanuts gets sent to school for your child’s lunch. If you are a parent of a child with a peanut allergy you understand how important and serious this is – your child is literally one errant Snickers bar away from death.
The general consensus is that food allergies have been on the rise in developed countries, although studies show a wide range of estimates based upon study techniques. A US review found the prevalence of self-reported peanut allergies ranged from 0-2%. A European review found the average estimate to be 2.2% – around 2% is usually the figure quoted. In a direct challenge study, at age 4, 1.1% of the 1218 children were sensitized to peanuts, and 0.5% had had an allergic reaction to peanuts. That means there are millions of people with peanut allergies.
So far there is no cure for the allergies themselves. Acute attacks can be treated with epinephrine, but there are cases of children dying (through anaphylaxis) even after multiple shots. The only real treatment is to obsessively avoid contact with the food in question. Peanuts, tree nuts, and shellfish are the good most likely to cause anaphylaxis.
There is, however, a potential solution. Researchers have been working for year on developing a cultivar of peanut that does not cause allergies. Attempts to achieve this through conventional breeding and hybridization have failed and does not seem likely to succeed. The only real hope of a hypoallergenic peanut is through genetic modification. We are, in fact, on the brink of achieving this goal, but anti-GMO fears are getting in the way.
There are 7 proteins that have been identified in peanuts that cause an allergic reaction. The allergic reaction from peanuts is entirely an IgE mediated Type I hypersensitivity response. The proteins crosslink with the IgE antibodies, which them bind to mast cells and basophils (cells in the immune system) causing a significant inflammatory response that clinically causes the allergic reaction. One peanut contains about 200mg of protein, and as little as 2mg is enough to cause objective symptoms of an allergic reaction.
What makes a food protein an allergen is interesting. About 700 amino acid sequences have been identified that help confer allergenicity to protein. These protein segments allow the protein to survive processing and digestion, and allow the protein to bind to IgE antibodies.
In 2005 a study was published showing that it is possible to silence the gene for the Ara H2 protein, the primary allergenic protein in peanuts. A 2008 follow up by the same team showed decreased allergenicity of the altered peanut. So where are our hypoallergenic peanuts? This is a complicated question, and I don’t think I can give a full answer.
The delay in marketing a hypoallergenic peanut seems to be due partly to technical issues – it turns out to be a lot more difficult to make the necessary changes than at first thought. However, it also seems to be due to the anti-GMO campaign, which has been scaring away investors and making politicians gun-shy.
A Japanese mathematician claims to have solved one of the most important problems in his field.
Sometime on the morning of 30 August 2012, Shinichi Mochizuki quietly posted four papers on his website. The papers were huge — more than 500 pages in all — packed densely with symbols, and the culmination of more than a decade of solitary work. They also had the potential to be an academic bombshell. In them, Mochizuki claimed to have solved the abc conjecture, a 27-year-old problem in number theory that no other mathematician had even come close to solving. If his proof was correct, it would be one of the most astounding achievements of mathematics this century and would completely revolutionize the study of equations with whole numbers.
Mochizuki, however, did not make a fuss about his proof. The respected mathematician, who works at Kyoto University's Research Institute for Mathematical Sciences (RIMS) in Japan, did not even announce his work to peers around the world. He simply posted the papers, and waited for the world to find out.
Probably the first person to notice the papers was Akio Tamagawa, a colleague of Mochizuki's at RIMS. He, like other researchers, knew that Mochizuki had been working on the conjecture for years and had been finalizing his work. That same day, Tamagawa e-mailed the news to one of his collaborators, number theorist Ivan Fesenko of the University of Nottingham, UK. Fesenko immediately downloaded the papers and started to read. But he soon became “bewildered”, he says. “It was impossible to understand them.”
Fesenko e-mailed some top experts in Mochizuki's field of arithmetic geometry, and word of the proof quickly spread. Within days, intense chatter began on mathematical blogs and online forums (see Nature http://doi.org/725; 2012). But for many researchers, early elation about the proof quickly turned to scepticism. Everyone — even those whose area of expertise was closest to Mochizuki's — was just as flummoxed by the papers as Fesenko had been. To complete the proof, Mochizuki had invented a new branch of his discipline, one that is astonishingly abstract even by the standards of pure maths. “Looking at it, you feel a bit like you might be reading a paper from the future, or from outer space,” number theorist Jordan Ellenberg, of the University of Wisconsin–Madison, wrote on his blog a few days after the paper appeared.
Three years on, Mochizuki's proof remains in mathematical limbo — neither debunked nor accepted by the wider community. Mochizuki has estimated that it would take an expert in arithmetic geometry some 500 hours to understand his work, and a maths graduate student about ten years. So far, only four mathematicians say that they have been able to read the entire proof.
Animal birth control could soon be just a shot away: A new injection makes male and female mice infertile by tricking their muscles into producing hormone-blocking antibodies. If the approach works in dogs and cats, researchers say, it could be used to neuter and spay pets and to control reproduction in feral animal populations. A similar approach could one day spur the development of long-term birth control options for humans.
“This looks incredibly promising,” says William Swanson, director of animal research at the Cincinnati Zoo and Botanical Garden in Ohio. “We’re all very excited about this approach; that it’s going to be the one that really works.”
For decades, the go-to methods for controlling animal reproduction have been spay or neuter surgeries. But the surgeries, which require animals to be anesthetized, can be expensive—one reason so many dogs and cats remain unfixed and feral animal populations continue to grow. Nearly 2.7 million dogs and cats were euthanized in U.S. shelters last year. A cheaper, faster method of sterilization is considered a holy grail for animal population control.
To get there, researchers have already created vaccines that trigger an immune response in animals. This response produces antibodies that block gonadotropin-releasing hormone (GnRH), required by all mammals to turn on the pathways that spur egg or sperm development. The vaccines in this class—including deer contraceptive GonaCon—have been shown to effectively work as both male and female birth control in animals. But, like many human immunizations, the vaccines rely on an immune response that eventually dwindles away, forcing the use of booster shots every few years.
Biologist Bruce Hay of the California Institute of Technology in Pasadena and colleagues took a different approach to blocking GnRH. Rather than rely on animals’ immune systems to create antibodies, he and his colleagues engineered a piece of DNA that—when packaged inside inactive virus shells and injected into mice—turned their muscle cells into anti-GnRH antibody factories. Because muscle cells are some of the longest lasting in the body, they continue to churn out the antibodies for 10 or more years. Both male and female mice with high enough levels of the antibodies were rendered completely infertile when Hay’s team allowed them to mate 2 months later, the team reports online today in Current Biology.
Via Integrated DNA Technologies
Over the last two decades, scientists have argued back and forth on whether or not ultra-small bacteria exist. The argument has been fueled, in part, by the1996 find of ultra-tiny fossil microorganisms on a meteorite from the planet Mars. But earlier this year, researchers at the University of California, Berkeley and the Department of Energy’s Lawrence Berkeley National Laboratory have captured detailed cryogenic electron microscopy images of ultra-small bacteria. These cells are now believed to be as small as a cell can get and still possess sufficient internal material needed to sustain life.
The first author of the study, Birgit Luef, is now a researcher at NTNU’s Department of Biotechnology. The publication was the result of her postdoctoral work at UC Berkeley. The researchers found several kinds of bacteria from three microbial phyla that are poorly understood. The bacteria were in groundwater and are thought to be quite common. But what surprised Luef and her colleagues was that the bacteria were close to and in some cases smaller than what many scientists have long considered the lower size limit of life. They reported the findings in the spring in the journal Nature Communications.
The cells had an average volume 0.009 ± 0.002 cubic microns, meaning 150 of the bacteria would fit inside a single cell of Escherichia coli.
Two scientists won the Nobel Prize in physics Tuesday for key discoveries about a cosmic particle that whizzes through space at nearly the speed of light, passing easily through Earth and even your body.
Takaaki Kajita of Japan and Arthur McDonald of Canada were honored for showing that these tiny particles, called neutrinos, have mass. That's the quality we typically experience as weight.
"The discovery has changed our understanding of the innermost workings of matter and can prove crucial to our view of the universe," the Royal Swedish Academy of Sciences said in awarding the prize.
The work dispelled the long-held notion that neutrinos had no mass. Neutrinos come in three types, or "flavors," and what the scientists actually showed is that neutrinos spontaneously shift between types. That in turn means they must have mass.
Via José Gonçalves, John Purificati
Human brains flexibly combine the meanings of words to compose structured thoughts. For example, by combining the meanings of “bite,” “dog,” and “man,” we can think about a dog biting a man, or a man biting a dog. In two functional magnetic resonance imaging (fMRI) experiments using multivoxel pattern analysis (MVPA), a team of scientists now identified a region of left mid-superior temporal cortex (lmSTC) that flexibly encodes “who did what to whom” in visually presented sentences. They found that lmSTC represents the current values of abstract semantic variables (“Who did it?” and “To whom was it done?”) in distinct subregions. Experiment 1 first identified a broad region of lmSTC whose activity patterns (i) facilitate decoding of structure-dependent sentence meaning (“Who did what to whom?”) and (ii) predicted affect-related amygdala responses that depend on this information (e.g., “the baby kicked the grandfather” vs. “the grandfather kicked the baby”). Experiment 2 then identified distinct, but neighboring, subregions of lmSTC whose activity patterns carry information about the identity of the current “agent” (“Who did it?”) and the current “patient” (“To whom was it done?”). These neighboring subregions lie along the upper bank of the superior temporal sulcus and the lateral bank of the superior temporal gyrus, respectively. At a high level, these regions may function like topographically defined data registers, encoding the fluctuating values of abstract semantic variables. This functional architecture, which in key respects resembles that of a classical computer, may play a critical role in enabling humans to flexibly generate complex thoughts.
Via Donald J Bolger
Researchers modify more than 60 genes in effort to enable organ transplants into humans.
For decades, scientists and doctors have dreamed of creating a steady supply of human organs for transplantation by growing them in pigs. But concerns about rejection by the human immune system and infection by viruses embedded in the pig genome have stymied research. Now, bymodifying more than 60 genes in pig embryos — ten times more than have been edited in any other animal — researchers believe they may have produced a suitable non-human organ donor.
The work was presented on 5 October 2015 at a meeting of the US National Academy of Sciences (NAS) in Washington DC on human gene editing. Geneticist George Church of Harvard Medical School in Boston, Massachusetts, announced that he and colleagues had used the CRISPR/Cas9 gene-editing technology to inactivate 62 porcine endogenous retroviruses (PERVs) in pig embryos. These viruses are embedded in all pigs’ genomes and cannot be treated or neutralized.It is feared that they could cause disease in human transplant recipients.
Church’s group also modified more than 20 genes in a separate set of pig embryos, including genes that encode proteins that sit on the surface of pig cells and are known to trigger a human immune response or cause blood clotting. Church declined to reveal the exact genes, however, because the work is as yet unpublished.Eventually, pigs intended for organ transplants would need both these modifications and the PERV deletions.
Via Integrated DNA Technologies
Age-related macular degeneration (AMRD) could be treated by transplanting photoreceptors produced by the directed differentiation of stem cells, thanks to findings published today by Professor Gilbert Bernier of the University of Montreal and its affiliated Maisonneuve-Rosemont Hospital. ARMD is a common eye problem caused by the loss of cones. Bernier's team has developed a highly effective in vitro technique for producing light sensitive retina cells from human embryonic stem cells. "Our method has the capacity to differentiate 80% of the stem cells into pure cones," Professor Gilbert explained. "Within 45 days, the cones that we allowed to grow towards confluence spontaneously formed organised retinal tissue that was 150 microns thick. This has never been achieved before."
In order to verify the technique, Bernier injected clusters of retinal cells into the eyes of healthy mice. The transplanted photoreceptors migrated naturally within the retina of their host. "Cone transplant represents a therapeutic solution for retinal pathologies caused by the degeneration of photoreceptor cells," Bernier explained. "To date, it has been difficult to obtain great quantities of human cones." His discovery offers a way to overcome this problem, offering hope that treatments may be developed for currently non-curable degenerative diseases, like Stargardt disease and ARMD. "Researchers have been trying to achieve this kind of trial for years," he said. "Thanks to our simple and effective approach, any laboratory in the world will now be able to create masses of photoreceptors. Even if there's a long way to go before launching clinical trials, this means, in theory, that will be eventually be able to treat countless patients."
How retroviruses like HIV spread in their hosts had been unknown — until a Yale team devised a way to watch it actually happen in a living organism. The elaborate and sometimes surprising steps the virus takes to reach and spread in the lymph nodes of a mouse have been captured on videos and described in the Oct. 2 issue of the journal Science.
“It’s all very different than what people thought,” said Walther Mothes, associate professor of microbial pathogenesis and co-senior author the paper.
Tracking fluorescently stained viruses in mice, the Yale team led by Mothes and co-senior author Priti Kumar, assistant professor of medicine and microbial pathogenesis, used sophisticated imaging technology to capture the action as the viral particles bind to macrophages via a sticky protein that is located at the capsule of the lymph node.
But that is only the first step of the journey. The captured viral particles open to a rare type of B-cell, seen in red in the accompanying movie. The virus particles then attach themselves to the tail of these B-cells and are dragged into the interior of the lymph node. In one to two days, these B-cells establish stable connections with tissue, enabling full transmission of the virus.
The insights provided by the videos identify a potential way to prevent HIV from infecting surrounding tissue. If researchers could develop a way to block the action of the sticky protein the virus uses to bind to macrophages, then the virus’ transmission could be halted, Mothes suggested.
In by far the majority of cancer cases, the doctor can quickly identify the source of the disease, for example cancer of the liver, lungs, etc. However, in about one in 20 cases, the doctor can confirm that the patient has cancer -- but cannot find the source. These patients then face the prospect of a long wait with numerous diagnostic tests and attempts to locate the origin of the cancer before starting any treatment.
Now, researchers at DTU Systems Biology have combined genetics with computer science and created a new diagnostic technology based on advanced self-learning computer algorithms which -- on the basis of a biopsy from a metastasis -- can with 85 per cent certainty identify the source of the disease and thus target treatment and, ultimately, improve the prognosis for the patient.
Each year, about 35,000 people are diagnosed with cancer in Denmark, and many of them face the prospect of a long wait until the cancer has been diagnosed and its source located. However, even after very extensive tests, there will still be 2-3 per cent of patients where it has not been possible to find the origin of the cancer. In such cases, the patient will be treated with a cocktail of chemotherapy instead of a more appropriately targeted treatment, which could be more effective and gentler on the patient.
The newly developed method, which researchers are calling TumorTracer, are based on analyses of DNA mutations in cancer tissue samples from patients with metastasized cancer, i.e. cancer which has spread. The pattern of mutations is analyzed in a computer program which has been trained to find possible primary tumor localizations. The method has been tested on many thousands of samples where the primary tumour was already identified, and it has proven extremely precise. The next step will be to test the method on patients with unknown primary tumours. In recent years, researchers have discovered several ways of using genome sequencing of tumours to predict whether an individual cancer patient will benefit from a specific type of medicine.
This is a very effective method, and it is becoming increasingly common to conduct such sequencing for cancer patients. Associate Professor Aron Eklund from DTU Systems Biology explains: "We are very pleased that we can now use the same sequencing data together with our new algorithms to provide a much faster diagnosis for cancer cases that are difficult to diagnose, and to provide a useful diagnosis in cases which are currently impossible to diagnose. At the moment, it takes researchers two days to obtain a biopsy result, but we expect this time to be reduced as it becomes possible to do the sequencing increasingly faster. And it will be straightforward to integrate the method with the methods already being used by doctors."
Sandia National Laboratories researchers seeking to make hydrogen a less expensive fuel for cars have upgraded a catalyst nearly as cheap as dirt — molybdenum disulfide, “molly” for short — to stand in for platinum, a rare element with the moonlike price of about $900 an ounce.
Sandia-induced changes elevate the plentiful, under-$2-per-ounce molly from being a welterweight outsider in the energy-catalyst field — put crudely, a lazy bum that never amounted to much — to a possible contender with the heavyweight champ.
The improved catalyst, expected to be the subject of an Oct. 7 Nature Communications paper, has already released four times the amount of hydrogen ever produced by molly from water. To Sandia postdoctoral fellow and lead author Stan Chou, this is just the beginning: “We should get far more output as we learn to better integrate molly with, for example, fuel-cell systems,” he said.
An additional benefit is that molly’s action can be triggered by sunlight, a feature which eventually may provide users an off-the-grid means of securing hydrogen fuel. Hydrogen fuel is desirable because, unlike gasoline, it doesn’t release carbon into the atmosphere when burned. The combustion of hydrogen with oxygen produces an exhaust of only water.
In Chou’s measured words, “The idea was to understand the changes in the molecular structure of molybdenum disulfide (MOS₂), so that it can be a better catalyst for hydrogen production: closer to platinum in efficiency, but earth-abundant and cheap. We did this by investigating the structural transformations of MOS₂ at the atomic scale, so that all of the materials parts that were ‘dead’ can now work to make H₂ [hydrogen].”
If you want to learn how something works, one strategy is to take it apart and put it back together again. For 10 years, a global initiative called the Blue Brain Project--hosted at the Ecole Polytechnique Federale de Lausanne (EPFL)--has been attempting to do this digitally with a section of juvenile rat brain. The project presents a first draft of this reconstruction, which contains over 31,000 neurons, 55 layers of cells, and 207 different neuron subtypes, on October 8 in Cell.
sing images from the NASA/ESA Hubble Space Telescope and ESO's Very Large Telescope, astronomers have discovered never-before-seen structures within a dusty disc surrounding a nearby star. The fast-moving wave-like features in the disc of the star AU Microscopii are unlike anything ever observed, or even predicted, before now. The origin and nature of these features present a new mystery for astronomers to explore. The results are published in the journal Nature on 8 October 2015.
AU Microscopii, or AU Mic for short, is a young, nearby star surrounded by a large disc of dust . Studies of such debris discs can provide valuable clues about how planets, which form from these discs, are created.
Astronomers have been searching AU Mic's disc for any signs of clumpy or warped features, as such signs might give away the location of possible planets. And in 2014 they used the powerful high-contrast imaging capabilities of ESO's newly installed SPHERE instrument, mounted on the Very Large Telescope for their search -- and discovered something very unusual.
"Our observations have shown something unexpected," explains Anthony Boccaletti of the Observatoire de Paris, France, lead author on the paper. "The images from SPHERE show a set of unexplained features in the disc which have an arch-like, or wave-like, structure, unlike anything that has ever been observed before."
Five wave-like arches at different distances from the star show up in the new images, reminiscent of ripples in water. After spotting the features in the SPHERE data the team turned to earlier images of the disc taken by the NASA/ESA Hubble Space Telescope in 2010 and 2011 to see whether the features were also visible in these . They were not only able to identify the features on the earlier Hubble images -- but they also discovered that they had changed over time. It turns out that these ripples are moving -- and very fast!
"We reprocessed images from the Hubble data and ended up with enough information to track the movement of these strange features over a four-year period," explains team member Christian Thalmann (ETH Zürich, Switzerland). "By doing this, we found that the arches are racing away from the star at speeds of up to about 40,000 kilometers/hour!"
Three scientists who developed therapies against parasitic infections have won this year's Nobel Prize in Physiology or Medicine.
Tu, who won a Lasker prize in 2011, developed the antimalarial drug artemisinin in the late 1960s and 1970s. She is the first China-based scientist to win a science Nobel. “This certainly is fantastic news for China. We expect more to come in the future,” says Wei Yang, president of the nation’s main research-funding agency, the National Natural Science Foundation of China.
In the 1960s, the main treatments for malaria were chloroquine and quinine, but they were proving increasingly ineffective. So in 1967, China established a national project against malaria to discover new therapies. Tu and her team screened more than 2,000 Chinese herbal remedies to search for drugs with antimalarial activity. An extract from the wormwood plant Artemisia annua proved especially effective and by 1972, the researchers had isolated chemically pure artemisinin.
That Tu won the Nobel prize is "great news", says Yi Rao, a neuroscientist at Peking University in Beijing who has researched the discovery of artemisinin. "I’m very happy about this. She totally deserves it.”
With a high-resolution structure of the mRNA-splicing machine now in hand, a new era of biological and pharmaceutical discovery is dawning.
Watching fruit flies buzz around the ripe bananas in your kitchen, you might think it’s a tad ludicrous, mortifying even, that humans have a similar number of genes—about 23,000—as the lowly insects. We are certainly more complex than Drosophila melanogaster, so what gives?
The answer lies in the spliceosome, a cellular machine that, at first glance, seems to do some pretty straightforward pruning of messenger RNA (mRNA).
As the cell transcribes your DNA’s nucleic acid sequence into RNA, the spliceosome lands on the newly forming mRNA strand, where it chops out unnecessary pieces, called introns, and joins together the leftover, essential sequences, called exons. The edited mRNA is then exported to the cell’s cytoplasm, where it gets translated into protein.
Most strands of unspliced mRNA, otherwise known as pre-mRNA, have about a dozen introns that can be removed. Yet the spliceosome doesn’t always link together the remaining exons in a straightforward manner. Sometimes the spliceosome intentionally skips an exon, or it reorders the exons, or it unexpectedly leaves an intron in the mix. On average, this variable editing process produces about 10 different proteins for every gene that we have. “Alternative splicing allows us to make the most out of every gene,” says Joan Steitz at Yale University School of Medicine. “Splicing is the reason we can have the same number of genes as the fruit fly Drosophila and yet be more complicated.”
This splice ‘n’ dice machine gives us our complexity, but it’s also exceedingly complex itself. So complex, in fact, that it’s taken decades and many twists and turns for scientists to figure out how it works. Because the spliceosome is so sophisticated, small hiccups in its operation can lead to biological malfunction and, ultimately, to disease. Discovery of the tiny machine has been a boon to drug developers, who are already developing drugs that target the spliceosome. They hope such molecules will treat the myriad diseases linked to splicing malfunction, including many cancers, some forms of blindness, and 10% of genetic diseases, such as spinal muscular atrophy and certain types of dwarfism.
What researchers now know is that cells assemble the spliceosome from an enormous cast of protein and RNA characters. These players work in unison, carrying out a gymnastics routine worthy of the Super Bowl halftime show. Five protein-RNA complexes, called ribonucleoproteins, and some 200 proteins come and go during different stages of human splicing. This machinery forms temporary assemblies that prep and then edit pre-mRNA, converting it into mRNA that can be read by the ribosome, another enormous ribonucleoprotein engine responsible for turning mRNA into protein.
Although it’s only about half the size of the ribosome, the spliceosome—with its ever-changing parts and rearrangements—is a much more dynamic machine, says Reinhard Lührmann of the Max Planck Institute for Biophysical Chemistry, in Göttingen, Germany. This has made the spliceosome one of structural biology’s most desirable targets and one of its most challenging foes: Many in the field say that the ribosome was a comparatively easy structure to solve, and even that was a feat so grand it earned the structural biologists who accomplished it a Nobel Prize.
So it was that scientists gasped in collective shock when a team of researchers—newcomers to the spliceosome field—published the first near-atomic-resolution structure of the splicing machinery in August. The scientists, led by Yigong Shi of Tsinghua University, in China, also published an accompanying paper on spliceosome function for good measure (Science 2015, DOI:10.1126/science.aac7629 and 10.1126/science.aac8159). “It was a total bombshell,” Yale’s Steitz says. “I never thought we’d see a complete structure this soon.”
Via Integrated DNA Technologies
The significant advance, by a team at the University of New South Wales (UNSW) in Sydney appears today in the international journal Nature.
"This makes the building of a quantum computer much more feasible, since it is based on the same manufacturing technology as today's computer industry," he added. The advance represents the final physical component needed to realize the promise of super-powerful silicon quantum computers, which harness the science of the very small - the strange behavior of subatomic particles - to solve computing challenges that are beyond the reach of even today's fastest supercomputers.
In classical computers, data are rendered as binary bits, which are always in one of two states: 0 or 1. However, a quantum bit (or 'qubit') can exist in both of these states at once, a condition known as a superposition. A qubit operation exploits this quantum weirdness by allowing many computations to be performed in parallel (a two-qubit system performs the operation on 4 values, a three-qubit system on 8, and so on). "If quantum computers are to become a reality, the ability to conduct one- and two-qubit calculations are essential," said Dzurak, who jointly led the team in 2012 who demonstrated the first ever silicon qubit, also reported in Nature.
But until now, it had not been possible to make two quantum bits 'talk' to each other - and thereby create a logic gate - using silicon. But the UNSW team - working with Professor Kohei M. Itoh of Japan's Keio University - has done just that for the first time. The result means that all of the physical building blocks for a silicon-based quantum computer have now been successfully constructed, allowing engineers to finally begin the task of designing and building a functioning quantum computer.
High levels of LDL cholesterol — the “bad” cholesterol — increase the risk of heart disease, the leading cause of death in the United States. A Yale-led research team has identified an RNA molecule that plays an important role in regulating cholesterol. Therapeutic targeting of this non-coding RNA markedly reduces LDL while boosting HDL, the good cholesterol.
The finding, published online ahead of print in Nature Medicine, may lead to new therapies designed to decrease high cholesterol and heart disease. The researchers used a high-throughput screening technique to identify which tiny RNA molecules, or microRNAs, influence LDL cholesterol levels in the blood. They found that a particular RNA, known as miR-148a, modifies LDL receptors in liver cells of both mice and humans. They also discovered that miR-148a suppresses a gene that is critical for controlling levels of HDL cholesterol.
“The key finding is the identification of another molecular target that could be used for treating high levels of bad cholesterol, and potentially treating cardiovascular disease,” said Carlos Fernandez-Hernando, associate professor of comparative medicine and pathology, and the study’s senior author. “By blocking this microRNA pharmacologically, we can reduce bad cholesterol.”
“Our work also establishes miR-148a as a promising therapeutic target to increase levels of good cholesterol,” noted Leigh Goedeke, a post-doctoral associate at Yale and lead author of the study. “We may have found a new treatment option to simultaneously reduce two risk factors of heart disease.”
Via Integrated DNA Technologies
Better diagnosis leads to better treatment – that’s well-known. Easier said than done, of course, since that’s not always possible when tests for diseases or infections take time to generate results, for example, or are inaccurate or insensitive. Take viruses: There is an abundance out there capable of causing disease, many of which can present similar symptoms or, perhaps worse, none at all. Detection can, therefore, be a bit of a nightmare, sometimes demanding a labor-intensive and costly suite of tests to get to the bottom of a case.
What if there was a universal, one-size-fits-all-test that could pick up any known virus in a sample, eliminating this time-consuming detective work? That might sound quite out of our clutches, but researchers at Washington University School of Medicine might just have achieved this long-awaited, eyebrow-raising feat.
“With this test, you don’t have to know what you’re looking for,” senior author Gregory Storch said in a statement. “It casts a broad net and can efficiently detect viruses that are present at very low levels. We think the test will be especially useful in situations where a diagnosis remains elusive after standard testing or in situations in which the cause of a disease outbreak is unknown.”
Describing their work in Genome Research, the results are pretty impressive. To make their “ViroCap,” the researchers began by creating a broad panel of sequences to be targeted by the test, which they generated using unique stretches of DNA or RNA found in viruses across 34 different human- and animal-infecting families. This resulted in millions of stretches of nucleic acid that can be used to capture matching strands in a sample, should they be present.
But the broad spectrum of this test is not its only remarkable quality: It’s so sensitive that it can even pick up slight variations in sequences, meaning that a virus’ subtype can also be identified – a feature not possible with many traditional tests. Although that wouldn’t necessarily change the way a patient is treated, it could aid disease surveillance.
To demonstrate its capabilities, the researchers took samples from a small group of patients at St. Louis Children’s Hospital and compared the results to those obtained from standard tests. While traditional sequencing managed to find viruses in the majority of the children, ViroCap also managed to pick up some common viruses that it had failed to detect. These included a flu virus and the virus responsible for chickenpox. In a second test run on a different group of children displaying fevers, the new test found an additional seven viruses to the 11 that the traditional testing managed to detect.
All of this sounds great on paper, but of course it is not yet ready to be used in the clinic. Further trials are required first to check its accuracy on larger groups of people, as so far only a limited number of patients have been screened. But when the time comes, the team plans to make it widely available, which would be welcome in the face of outbreaks like Ebola. Furthermore, the team ultimately hopes to tweak it so that it can detect genetic material from other microbes, like bacteria. If that’s possible, we could have a seriously useful machine on our hands that could change diagnostic medicine for the better.
Harvard-affiliated researchers have designed a specialized catheter for fixing holes in the heart by using a biodegradable adhesive and patch. The team reported in the journal Science Translational Medicine that the catheter has been used successfully in animal studies to help close holes without requiring open-heart surgery.
Pedro del Nido, chief of cardiac surgery at Boston Children’s Hospital, the William E. Ladd Professor of Child Surgery at Harvard Medical School, and contributing author on the study, said the device represents a radical change in the way some kinds of cardiac defects are repaired. “In addition to avoiding open-heart surgery, this method avoids suturing into the heart tissue, because we’re just gluing something to it.”
Catheterizations are preferable to open-heart surgery because they don’t require stopping the heart, putting the patient on bypass, and cutting into the heart. The Heart Center at Boston Children’s is working toward the least invasive methods possible to correct heart defects, which are among the most common congenital defects.
Last winter, news of the unique adhesive patch was published in the same journal as the latest report. This represented a large step forward in the quest to reduce complications associated with repairing heart defects. While medical devices that remain in the body may be jostled out of place or fail to cover the hole as the body grows, the patch allows the heart tissue to create its own closure, and then it dissolves.
To truly realize the patch’s potential, however, the research team sought a way to deliver the patch without open-heart surgery. Their catheter device utilizes UV-light technology and can be used to place the patch in a beating heart.
The catheter is inserted through a vein in the neck or groin and directed to the defect within the heart. Once the catheter is in place, the clinician opens two positioning balloons: one around the front end of the catheter, passing through the hole, and one on the other side of the heart wall. The clinician then deploys the patch and turns on the catheter’s UV light.
The light reflects off of the balloon’s shiny interior and activates the patch’s adhesive coating. As the glue cures, pressure from the positioning balloons on either side of the patch help secure it in place. Finally, both balloons are deflated, and the catheter is withdrawn. Over time, normal tissue growth resumes, and heart tissue grows over the patch. The patch itself dissolves when it is no longer needed.
The Nobel prize in chemistry has been awarded to Tomas Lindahl, Paul Modrich and Aziz Sancar for their research into the mechanisms that cells use to repair DNA.
From the moment an egg is fertilized it begins to divide. Two cells become four, four cells become eight. After one week a human embryo consists of 128 cells, each with its own set of genetic material. Unravel all that DNA and it would stretch for 300 meters. But many billions more divisions take place on the path to adulthood, until we carry enough DNA in our trillions of cells to reach 250 times to the sun and back. The most remarkable feat is how the genetic information is copied so faithfully. “From a chemical perspective, this ought to be impossible,” the Nobel committee said.
“All chemical processes are prone to random errors. Additionally, your DNA is subjected on a daily basis to damaging radiation and reactive molecules. In fact, you ought to have been a chemical chaos long before you even developed into a foetus,” they added.
Lindahl, Modrich and Sancar worked out how cells repair faults that inevitably creep in when DNA is copied time and time again, and mutations that arise under a barrage of environmental factors such as UV rays in sunlight.
Towards the end of the 1960s, many scientists considered DNA to be incredibly stable. But working at the Karolinska Institute in Stockholm, Lindahl worked out that there must be thousands of potentially damaging attacks on the genome every day – an onslaught that would make human life impossible.
Working with bacterial DNA, Lindahl began the search for enzymes that repair faulty genetic mateial. He focused on a weakness in the way the DNA letters, G, T, C and A, pair up. Normally, C (cytosine) pairs only with G (guanine), but C can lose an amino group which makes it pair up with A ( adenine) instead. If the mis-pairing stands, it creates a mutation the next time it is copied. Lindahl realised that cells must have a way to protect themselves from such a fate, and published details of the enzyme responsible in 1974.
Lindahl moved to the UK in the 1980s and became director of what is now Cancer Research UK’s Clare Hall Laboratory, a place known for its scientific creativity. There he worked out, step by step, the DNA repair processes in humans.
But DNA can also be disrupted by environmental factors, such as UV radiation. How organisms survived these mutations piqued the interest of Sancar who noticed that bacteria exposed to deadly doses of UV could repair themselves if lit up blue light. At the University of Texas in Dallas, he discovered an enzyme called photolyase that repairs UV-damaged DNA.
At Yale University, Sancar went on to identify enzymes that spot UV damage and then cut the DNA to remove the faulty genetic code. Later, at the University of North Carolina in Chapel Hill, he mapped the equivalent repair process in humans.
Cutting-edge gene-editing techniques have produced an unexpected byproduct — tiny pigs that a leading Chinese genomics institute will soon sell as pets.
BGI in Shenzhen, the genomics institute that is famous for a series of high-profile breakthroughs in genomic sequencing, originally created the micropigs as models for human disease, by applying a gene-editing technique to a small breed of pig known as Bama. On 23 September 2015, at the Shenzhen International Biotech Leaders Summit in China, BGI revealed that it would start selling the pigs as pets. The animals weigh about 15 kilograms when mature, or about the same as a medium-sized dog.
At the summit, the institute quoted a price tag of 10,000 yuan (US$1,600) for the micropigs, but that was just to "help us better evaluate the market”, says Yong Li, technical director of BGI’s animal-science platform. In future, customers will be offered pigs with different coat colors and patterns, which BGI says it can also set through gene editing.
With gene editing taking biology by storm, the field's pioneers say that the application to pets was no big surprise. Some also caution against it. “It's questionable whether we should impact the life, health and well-being of other animal species on this planet light-heartedly,” says geneticist Jens Boch at the Martin Luther University of Halle-Wittenberg in Germany. Boch helped to develop the gene-editing technique used to create the pigs, which uses enzymes known as TALENs (transcription activator-like effector nucleases) to disable certain genes.
How to regulate the various applications of gene-editing is an open question that scientists are already discussing with agencies across the world. BGI agrees on the need to regulate gene editing in pets as well as in the medical research applications that make up the core of its micropig activities. Any profits from the sale of pets will be invested in this research. “We plan to take orders from customers now and see what the scale of the demand is,” says Li.
The decision to sell the pigs as pets surprised Lars Bolund, a medical geneticist at Aarhus University in Denmark who helped BGI to develop its pig gene-editing programme, but he admits that they stole the show at the Shenzhen summit. “We had a bigger crowd than anyone,” he says. “People were attached to them. Everyone wanted to hold them.”
They could meet a preexisting demand. In the United States, for instance, reports have surfaced of people who wanted a porcine lap pet, but were disappointed when animals touted as 'teacup' pigs weighing only 5 kilograms grew into 50-kilogram animals. Genetically-edited micropigs stay reliably small, the BGI team says.
A team of researchers with members from the University of California and Rice University has found a way to get a flat transistor to defy theoretical limitations on Field Effect Transistors (FETs). In their paper published in the journal Nature, the team describes their work and why they believe it could lead to consumer devices that have both smaller electronics and longer battery life. Katsuhiro Tomioka with Erasmus MC University Medical Center in the Netherlands offers a News & Views article discussing the work done by the team in the same journal edition.
As Tomioka notes, the materials and type of architecture currently used in creating small consumer electronic devices is rapidly reaching a threshold upon which a tradeoff will have to be made—smaller transistors or more power requirements—this is because of the unique nature of FETs, shortening the channel they use requires more power, on a logarithmic scale. Thus, to continue making FETs ever smaller and to get them to use less power means two things, the first is that a different channel material must be found, one that allow high switch-on currents at low voltages. The second is a way must be found to lower the voltage required for the FETs.
Researchers have made inroads on the first requirement, building FETs with metal-oxide-semiconductor materials, for example. The second has proved to be more challenging. In this latest effort, the researchers looked to tunneling to reduce voltage demands, the results of which are called, quite naturally, tunneling FETs or TFETs—they require less voltage because they are covered (by a gate stack) and work by transporting a charge via quantum-tunneling. The device the team built is based on a 2D bilayer of molybdenum disulfide and bulk germanium—it demonstrated a negative differential resistance, a marker of tunneling, and a very steep subthreshold slope (the switching property associated with rapid turn-on) which fell below the classical theoretical limit.
The work by the team represents substantial progress in solving the miniturization problem for future electronics devices, but as the team notes, there is still much to do. They express optimism that further improvements will lead to not just better consumer devices, but tiny sensors that could be introduced into the body to help monitor health.