#Lexus Hoverboard Gets Off The Ground By Michael Greshko, Inside Science-In the classic 1989 film Back to the Future 2,
intrepid time traveler Marty Mcfly jumps ahead a few decades, to October 21, 2015. Luxury car manufacturer Lexus appears to be ready for him.
This week, they announced that they've built a"real, rideable"hoverboard. They've even released video of it,
oozing fog and mysteriously floating over what looks like a concrete sidewalk. Check out the 38-second teaser for yourself:
Lexus has no plans to sell the prototype board, Ars Technica reports. But even so, it's really floating there!
And on the hoverboard's official website, Lexus hints at how they pulled it off:
The Lexus Hoverboard uses magnetic levitation to achieve amazing frictionless movement. Liquid nitrogen cooled superconductors and permanent magnets combine to allow Lexus to create the impossible.
Now, Lexus, your hoverboard is really cool, but"impossible"?"Let's not get ahead of ourselves. Levitation is not only possible but also well understood from a physics perspective.
Lexus is taking advantage of key properties of materials called superconductors. As you might expect,
these sorts of materials are"super"at conducting electricity: When superconductors are cooled below a certain temperature,
their electrons buddy up and move through the material without encountering any sort of resistance. More specifically, Lexus'use of liquid nitrogenhich has a temperature of-321 degrees Fahrenheitells us that they're using a high-temperature superconductor like yttrium barium copper oxide,
which is perfect for the kind of levitation Lexus is (Tony?)hawking. Yes,"liquid nitrogen"and"high-temperature"correctly went in the same sentence.
Lexus'superconductor probably starts working at about-292 degrees Fahrenheit, which sounds unfathomably cold. However, this temperature is actually quite warm by superconductor standards.
The first superconductor ever discovered, in 1911, had to be cooled down to-452 degrees Fahrenheit, only a few degrees warmer than absolute zero, the coldest possible temperature.
So how did Lexus float its high-temperature superconductors? By playing a magnetic trick on them.
When a high-temperature superconductor is too warm to work, magnetic fields can pass right through it without a problem.
But if you then cool the superconductor down so that it starts working, it gets"stuck"on the magnetic field lines that were passing through it,
as if it were caught in a magnetic spiderweb. In other words, superconductors"freeze the flux lines of the field,
"says Steve Gourlay, the head of the Lawrence Berkeley National Lab's Superconducting Magnet Group, leaving the superconductor embedded in the magnetic field at that particular location.
A cross-section of a high-temperature superconductor (blue rectangle)" embedded"in a magnetic field (black lines. The magnetic channels through the superconductor are called"quantum vortices."
"How cool is that?(Wikimedia Commons) To levitate the superconductor, all you need to do is embed the superconductor in the magnetic field a couple of inches above some kind of magnetic surface.
If you tried to move the superconductor, you'd kickstart circular eddies of electrical current on the superconductor's surface,
spawning miniature magnetic fields that work to the superconductor in place. These eddy currents even oppose gravity,
pushing off of the surface's magnetic field to keep the superconductor floating in midair. In normal conducting material such as copper,
which resists the flow of electricity, those eddies would weaken. The lack of electrical resistance in superconductors means that once an eddy current starts
nothing can sap its strength. As long as you keep the superconductor cold, it'll stay floating above a magnet,
its eddy currents fighting gravity to a Draw in short, Lexus has come up with a cool way to use superconductors to levitate a hoverboard and its rider, an impressive achievement,
if true--Lexus hasn't provided video of someone riding the board. But by now, you've probably noticed a theme:
levitation happens when the superconductor interacts with an outside magnetic field. And this is where Lexus is giving us a little movie magic.
If the superconductors are in the hoverboard, then we need an outside magnetic field for the hoverboard to coast on.
This is where Lexus'"permanent magnets"come in. Gourlay suspects that Lexus laid down a bunch of very strong rare-earth magnets underneath the"sidewalk,
"setting up a magnetic field powerful enough to support both board and, Lexus promises, a rider.
In fact, Gizmodo reports that the hoverboard only works on"special metallic surfaces.""This sort of setup is probably too expensive for your everyday skate park.
Rare-earth magnets"can be, oh, I don't know, $100 a kilogram?""Gourlay said.""It isn't cheap."
"So unless you plan on covering your driveway with thousands of dollars'worth of magnets,
this cleverly made hoverboard wouldn't even get you out of your garage. Even so, Gourlay is intrigued by the prospect of using superconductorshich are used in everything from maglev trains to the Large Hadron Collidern something like a hoverboard."
"I couldn't ride it without breaking my neck, "he said, "but that would be kind of cool."
"Michael Greshko is a science writer based in Washington, D c, . who has written for NOVA Next, the National Academies,
and NYTIMES. com, among other outlets. He tweets at@michaelgreshko. Reprinted with permission from Inside Science, an editorially independent news product of the American Institute of Physics,
a nonprofit organization dedicated to advancing, promoting and serving the physical sciences c
#Glaxosmithkline Gene Discovery In Poppies Paves Way For Better Painkillers A long sought after gene that is a critical gateway step in the synthesis of the morphinan class of alkaloids,
which include the painkiller drugs morphine and codeine, has been discovered. The gene, called STORR, is only found in poppy species that produce morphinans.
The STORR gene evolved when two other genes encoding oxidase and reductase enzymes came together millions of years ago.
The resulting gene fusion plays a key role in production of morphine. The researchers hope this will enable the breeding of bespoke poppy varieties
including those that produce the anticancer compound noscapine. Discovery of the STORR gene completes the set of genes needed for genetic engineering of morphine production in microbes such as yeast.
Whether or not this can compete commercially with plant based production remains to be seen. The scientists identified poppy plants that were not able to produce morphine or codeine but instead accumulated another compound called (S)- reticuline.
These plants were found to carry mutations in the STORR gene. These mutations cause a roadblock in the pathway to morphine production in poppy plants.
The scientists were able to show that the non-mutated wild type gene can overcome the roadblock
by expressing it in yeast cells. The naturally occurring opiates of the morphinan class of alkaloids include morphine, codeine and thebaine.
Morphine and codeine can be used directly as analgesic painkillers. Thebaine is used widely as the starting point for synthesis of a number of semisynthetic opiates including hydrocodone, hydromorphone, oxycodone, and oxymorphone.
Thebaine is used also to synthesise the opioid antagonist naloxone, which is used to counter the effects of opiate overdose.
The discovery of the STORR gene completes the suite of genes thought to be required for production of morphinans in microbial systems.
he discovery of the STORR gene provides us with a new tool for molecular plant breeding,
orphinan biosynthesis in opium poppy requires a P450-oxidoreductase fusion protein Science Express n
#Oscillatory Chemical reactions: What Your Clothes May Literally Say About You In the future Wearing a computer on your sleeve may be a lot cooler than a plastic watch with an Apple logo on it-researchers at the University of Pittsburgh have designed a responsive hybrid material fueled by an oscillatory chemical reactions.
They can even perform computations based on changes in the environment or movement, and respond to human vital signs.
The material system is sufficiently small and flexible enough to be integrated into fabric or introduced as an inset into a shoe.
distinguished professor of chemical and petroleum engineering, and Steven P. Levitan, Ph d.,John A. Jurenko professor of electrical and computer engineering, integrated models for self-oscillating polymer gels and piezoelectric micro-electric-mechanical systems to devise a new
reactive material system capable of performing computations without external energy inputs, amplification or computer mediation. The studies combine Balazs'research in Belousov-Zhabotinsky (BZ) gels, a substance that oscillates in the absence of external stimuli,
and Levitan's expertise in computational modeling and oscillator-based computing systems. By working with Dr. Victor V. Yashin, research assistant professor of chemical
and petroleum engineering and lead author on the paper, the researchers developed design rules for creating a hybrid"BZ-PZ"material."
"allowing the material to be used for computation. Levitan adds, however, the computations would not be general purpose,
but rather specific to pattern-matching and recognition, or other non-Boolean operations.""Imagine a group of organ pipes,
and respond accordingly, thereby performing the actual computing.""Developing so-called"materials that compute"addresses limitations inherent to the systems currently used by researchers to perform either chemical computing or oscillator-based computing.
Chemical computing systems are limited by both the lack of an internal power system and the rate of diffusion as the chemical waves spread throughout the system,
enabling only local coupling. Further, oscillator-based computing has not been translated into a potentially wearable material.
The hybrid BZ-PZ model, which has never been proposed previously, solves these problems and points to the potential of designing synthetic material systems that are powered self.
#Eye disease Detected-Using A Smartphone Researchers at the Medical and Surgical Center for Retina have developed software that detects eye diseases such as diabetic macular edema using a smartphone.
The technology was designed for general physicians who support the health system in Mexico to detect certain abnormalities without an ophthalmologist
and send the patient to the specialist. It's obviously better and cheaper to prevent blindness rather than try to cure it so an app on a cellphone that just needs to focus on the eye is better in all ways.
This is especially important in rural communities where expertise areas such as ophthalmology won't be commonly available. The software was developed in collaboration with biomedical engineers from the ITESM
and uses the camera of the phone to detect any abnormality in the thickness of the retina."
"The idea is to detect and prevent diseases in general practice. We are not replacing the specialist,
we want to know which patients have a disease and make an early detection, "says Dr. Juan carlos Altamirano Vallejo, medical director of the Medical and Surgical Center for Retina."
"It will help those that when they go to the eye doctor are already blind, we needed to go a step back,
to know who is at risk and needs to go to a specialist. Not wait for a doctor."
"The Medical and Surgical Center for Retina is a small group with ten people dedicated to ophthalmology and retina special medical care.
It it also dedicated to biomedical and pharmaceutical research, to develop diagnostics and equipment, applicable to society.
They expect it to be marketed soon n
#New GHOST Technology Leaps Out Of The Screen Nothing will make you feel like Tony Stark more than being able to change the shape of displays with your hands,
pulling objects and data out of the screen and playing with them in mid-air.
Right now that's just in an Avengers movie. Instead, we live in a world of flat-screen displays,
even though the real world is not flat, it has hills and valleys, people and objects. Being able to manipulate a display
and drag features into a 3-D world is the purpose of GHOST (Generic, Highly-Organic Shape-Changing Interfaces), an EU research project designed to tap humansability to reason about
and manipulate physical objects through the interfaces of computers and mobile devices.""This will have all sorts of implications for the future,
from everyday interaction with mobile phones to learning with computers and design work,"says GHOST coordinator Professor Kasper Hornbaek of the University of Copenhagen."
"It not only about deforming the shape of the screen, but also the digital object you want to manipulate, maybe even in mid-air.
Through ultrasound levitation technology, for example, we can project the display out of the flat screen.
And thanks to deformable screens we can plunge our fingers into it.""This breakthrough in user interaction with technology allows us to handle objects,
and even data, in a completely new way. A surgeon, for instance, will be able to work on a virtual brain physically, with the full tactile experience,
before performing a real-life operation. Designers and artists using physical proxies such as clay can mold
and remold objects and store them in the computer as they work. GHOST researchers are also working with deformable interfaces such as pads and sponges for musicians to flex to control timbre, speed and other parameters in electronic music.
GHOST has produced an assembly line of prototypes to showcase shape-changing applications. mergeis one which allows data in bar charts to be pulled out of the screen by fingertips.
The information, whether it election results or rainfall patterns, can then be reordered and broken down by column, row or individually,
in order to visualize it better. The researchers have also been working with orphees flexible mobile devices with lycra or alloy displays
which bend and stretch according to use. These can change shape automatically to form screens to shield your fingers
when you type in a pincode, for example, or to move the display to the twists and turns of a game.
And such devices can be enlarged in the hand to examine data closer and shrunk again for storing away in a case or pocket.
One of the GHOST partners the University of Bristol, has spun off a startup, now employing 12 people, called Ultrahaptics,
to develop technology being studied in GHOST that uses ultrasound to create feeling in mid-air.
The company has attracted seed investment in the UK and further funding from the Horizon 2020 program 2
#Toward A Universal Flu Vaccine Flu vaccines can be shot a in the dark-they must be given yearly
and there's no guarantee the strains against which they protect will be the ones circulating once the season arrives.
New research suggests it may be possible to harness a previously unknown mechanism within the immune system to create more effective and efficient vaccines against this ever-mutating virus. In a Cell paper,
a team describes a new strategy that revolves around antibodies, immune proteins that target specific foreign proteins, called antigens.
One end of the antibody latches on to an antigen the other end, called the Fc region,
binds to immune cells and so helps coordinate the immune response.""While the conventional flu vaccine protects only against specific strains, usually three of them,
our experiments show that by including modified antibodies within the vaccine it may be possible to elicit broad protection against many strains simultaneously,
"says senior study author Jeffrey Ravetch, professor of Molecular genetics and Immunology at Rockefeller University.""We believe these results may represent a preliminary step toward a universal flu vaccine,
one that is effective against a broad range of the flu viruses."It was known already that chemical modifications to antibodies'Fc region altered their interactions with immune cells,
including B cells, which produce antibodies. In experiments that began with human volunteers, the team, led by Taia Wang, an instructor in clinical investigation,
and Jad Maamary, a post-doc, both in Ravetch's lab, investigated how changes to this region might be used to bolster an immune response:
namely the production of more potent antibodies against the flu virus. Every year in the United states, influenza is implicated in the deaths of thousands of people, mostly 65 and older,
and causes serious disease in many others. The virus makes for a difficult target for vaccines
because its strains are so diverse, and new ones are constantly emerging. Types A and B cause seasonal flu epidemics.
Influenza a viruses are broken further down into subtypes based in part on their surface proteins, which include hemagglutinin, the"H"in H1n1, for example.
The subtypes are divided further into strains. Currently most flu vaccines in the United states are formulated to target a total of three or four viral strains:
H1 and H3 Influenza a viruses, plus Influenza b virus strains. The strains are selected based on public health experts'predictions for the coming flu season.
But sometimes they are wrong, rendering the shots ineffective. A universal flu vaccine has become something of a holy grail,
and a number of strategies have been proposed to create it. Work in the Ravetch lab suggests a new alternative:
chemical modifications to the Fc region of antibodies. These regions go on form complexes with vaccine antigens,
which then modulate the evolving vaccine response. First, the researchers vaccinated healthy volunteers with a seasonal flu vaccine containing an inactivated strain of the H1n1 virus. They then tracked the volunteers'immune responses via blood samples,
keeping an eye out for chemical modifications to antibodies against the hemagglutinin protein. About seven days after the vaccination, they saw a spike in sialylated antibodies, meaning sialic acid,
an important signaling molecule, had been added at a specific spot on the Fc region. The greater the sialylation
the better a person's response to the vaccine. To tease apart how this chemical modification improves the immune response,
the researchers used cell cultures and mice to study the effects of sialylated Fc regions binding to B cells.
Their experiments revealed a complex interaction that ultimately pushes the B cells to produce antibodies with a higher affinity to their antigens.
It begins when a sialylated Fc region binds to a receptor protein known as CD23 on the B cells,
RIIB, which, in turn, discourages B cells producing low affinity antibodies. In this way, the sialylation on Fc regions establishes a high threshold for the immune response,
so that only B cells producing the highest affinity antibodies are activated. The result of the higher affinity was broad protection against H1 subtype influenza viruses. The researchers then used this knowledge to improve the vaccine itself.
They modified the H1n1 vaccine so it contained not only protein from the virus itself, but also sialylated antibodies against that protein."
"When we immunized mice with just the H1 protein from one strain or with the sialylated complexes containing the same viral protein,
we found both offered equal protection against the same strain of flu. However, when we exposed them to strains expressing different versions of the H1 protein,
only the sialylated immunizations offered protection, "Maamary says.""This was no small accomplishment, because H1 viruses can vary significantly from one another.""
which a vaccine containing sialylated antibodies elicits broadly protective antibodies, could potentially be harnessed to reduce the tremendous morbidity
and mortality caused by seasonal influenza virus infections, "Wang says.""We are now looking into applying this strategy toward improving existing vaccines;
ideally, this would result in a vaccine that provides life long immunity against flu infections. s
#Human Antibody Blocks Dengue virus In Mice Researchers have discovered that a human antibody specific to dengue virus serotype 2,
called 2d22, protects mice from a lethal form of the virus --and they suggest that the site where 2d22 binds to the virus could represent a potential vaccine target.
The mosquito-borne virus, which infects nearly 400 million people around the world each year, has four distinct serotypes,
and there is currently no protective vaccine available. Recent phase 3 clinical trials of a potential vaccine candidate showed poor efficacy,
especially against dengue virus serotype 2. Guntur Fibriansah and colleagues found that 2d22 protects mice against dengue virus serotype 2,
or after the rodents are inoculated with the virus. This finding suggests that the antibody may act as both a preventative and a therapeutic agent.
To learn more, the researchers analyzed cryo-electron microscopy (CRYO EM) structures of 2d22 in complex with two different strains of viral serotype 2--the dengue serotype with the most dynamic surface--at 6. 5
These CRYO EM structures reveal that 2d22 binds to viral envelope proteins, locking about two-thirds of them in place on the viral surface and preventing them from reorganizing into the orientations required to enter host cells.
"CRYO EM structure of an antibody that neutralizes dengue virus type 2 by locking E protein dimers,"by G. Fibriansah;
S m. Lok at Duke-National University of Singapore Graduate Medical school in Singapore; G. Fibriansah; T s. Ng;
S m. Lok at National University of Singapore in Singapore; K. D. Ibarra; E. Harris at University of California, Berkeley in Berkeley, CA;
S. A. Smith; J. E. Crowe Jr. at Vanderbilt University in Nashville, TN; A m. de Silva at University of North carolina School of medicine in Chapel hill, NC C
#Gene therapy Restores Hearing In Deaf Mice Using gene therapy, researchers at Boston Children's Hospital and Harvard Medical school have restored hearing in mice with a genetic form of deafness.
Their work, published online July 8 by the journal Science Translational Medicine, could pave the way for gene therapy in people with hearing loss caused by genetic mutations."
"Our gene therapy protocol is not yet ready for clinical trials--we need to tweak it a bit more
--but in the not-too-distant future we think it could be developed for therapeutic use in humans,
"says Jeffrey Holt, Phd, a scientist in the Department of Otolaryngology and F. M. Kirby Neurobiology Center at Boston Children's and an associate professor of Otolaryngology at Harvard Medical school.
Sensory hair cells in the cochlea of a Beethoven mouse treated with TMC2 gene therapy. In this confocal microscopy image, microvilli are shown in red and cell bodies in green.
Image: Charles Askew More than 70 different genes are known to cause deafness when mutated. Holt, with first author Charles Askew and colleagues at École Polytechnique Fédérale de Lausanne in Switzerland, focused on a gene called TMC1.
They chose TMC1 because it is a common cause of genetic deafness, accounting for 4 to 8 percent of cases,
and encodes a protein that plays a central role in hearing, helping convert sound into electrical signals that travel to the brain.
The researchers tested gene therapy in two types of mutant mice. One type had the TMC1 gene completely deleted
and is a good model for recessive TMC1 mutations in humans: Children with two mutant copies of TMC1 have profound hearing loss from a very young age, usually by around 2 years.
The other type of mouse, called Beethoven, has a specific TMC1 mutation--a change in a single amino acid
--and is a good model for the dominant form of TMC1-related deafness. In this form, less common than the recessive form, a single copy of the mutation causes children to gradually go deaf beginning around the age of 10 to 15 years.
To deliver the healthy gene, the team inserted it into an engineered virus called adeno-associated virus 1,
or AAV1, together with a promoter--a genetic sequence that turns the gene on only in certain sensory cells of the inner ear known as hair cells.
They then injected the gene-bearing AAV1 into the inner ear, with these findings: In the recessive deafness model, gene therapy with TMC1 restored the ability of sensory hair cells to respond to sound--producing a measurable electrical current--and also restored activity in the auditory portion of the brainstem.
Most importantly, the deaf mice regained their ability to hear. To test hearing, the researchers placed the mice in a"startle box
"and sounded abrupt, loud tones.""Mice with TMC1 mutations will just sit there, but with gene therapy, they jump as high as a normal mouse,
"says Holt. The force of their jump was measured by a plate on the floor underneath them;
it was detectable at sounds beginning around 80 decibels. In the dominant deafness model, gene therapy with a related gene, TMC2, was successful at the cellular and brain level,
and partially successful at restoring actual hearing in the startle test. Clinical trials on the horizon AAV1 is considered safe as a viral vector
and is already in use in human gene therapy trials for blindness, heart disease, muscular dystrophy and other conditions.
The researchers screened various types of AAV and various types of promoters to choose the best-performing combination.
They plan to further optimize their protocol and follow their treated mice to see if they retain hearing longer than the two months already observed.
Holt hopes to partner with clinicians at Boston Children's Department of Otolaryngology and elsewhere to start clinical trials of TMC1 gene therapy within 5 to 10 years."
"Current therapies for profound hearing loss like that caused by the recessive form of TMC1 are hearing aids,
and cochlear implants,"says Margaret Kenna, MD, MPH, a specialist in genetic hearing loss at Boston Children's Hospital who is familiar with the work."
"Cochlear implants are great, but your own hearing is better in terms of range of frequencies, nuance for hearing voices, music and background noise,
and figuring out which direction a sound is coming from. Anything that could stabilize or improve native hearing at an early age is really exciting
"Holt believes that other forms of genetic deafness may also be amenable to the same gene therapy strategy.
Overall, severe to profound hearing loss in both ears affects 1 to 3 per 1, 000 live births.""I can envision patients with deafness having their genome sequenced and a tailored,
precision medicine treatment injected into their ears to restore hearing, "Holt says. Sound transducers: How TMC works Holt's team showed in 2013 that TMC1
and the related protein TMC2 are critical for hearing, ending a rigorous 30-year search by scientists.
Sensory hair cells in the inner ear contain tiny projections called microvilli, each with a channel at its tip formed by TMC1 and TMC2 proteins.
a mutation in the TMC1 gene is sufficient to cause deafness. However, Holt's study also showed that gene therapy with TMC2 could compensate for loss of a functional TMC1 gene,
restoring hearing in the recessive deafness model and partial hearing in the dominant deafness model."
"This is a great example of how the basic science can lead to clinical therapies, "says Holt."
"The implications of successful gene therapy are profound, and we are delighted to be associated with this study program,
"says Ernesto Bertarelli, co-chair of the Bertarelli Foundation, the primary funder of the research."
"These findings mark a defining moment in the way we understand, and can ultimately challenge, the burden of deafness in humans.
The results are testament to the immense dedication of the research team and their commitment to bringing best-in-class science ever closer to real-world application. i
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