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DNA sequencing with nanopores reaches new lengths

DNA sequencing with nanopores reaches new lengths | Amazing Science | Scoop.it

Researchers from the University of Washington’s Departments of Physics and Genome Sciences have developed a nanopore sequencing technique reaching read lengths of several thousand bases. The result is the latest in a series of advances in nanopore technology developed at the university.


The team, led by Jens Gundlach, published their findings in Nature Biotechnology as an advanced online publication on June 25, 2014 ("Decoding long nanopore sequencing reads of natural DNA").


“This is the first time anyone has shown that nanopores can be used to generate interpretable signatures corresponding to very long DNA sequences from real-world genomes,” said co-author Jay Shendure, an associate professor in Genome Sciences, “It’s a major step forward.


”The idea for nanopore sequencing originated in the 90s: a lipid membrane, similar to the material that makes up the cell wall, acts as a barrier separating two liquids. Inserted into the membrane is a tiny gap, just nanometers across, called a nanopore. By applying a voltage difference across the barrier, ions in the liquid try to move between the two sides of the barrier and the only way to do this is to flow through the nanopore. The movement of the charged molecules between the two liquids is a current, just like electrons moving along a wire in an electrical circuit, and can be recorded.


Any DNA in the system is also pulled towards the other side of the barrier by the voltage difference, since DNA is negatively charged, and just like the ions it has to pass through the nanopore. The difference is that the DNA is much bigger than the ions and partially blocks the nanopore, making it harder for the smaller molecules to pass through. As the ions are blocked by the DNA, there is a measurable difference in the current flowing across the membrane which is dependent on the DNA base passing through the nanopore. By measuring the changing current, information can be gained on the bases passing through.


The researchers created the nanopore by inserting a single protein called Mycobacterium smegmatis porin A, or MspA, in the membrane. MspA is normally found lining the membrane of a species of bacteria, controlling the intake of nutrients.


One challenge the researchers faced was the control of the DNA passing through the nanopore. Normally, the DNA would zip through the MspA nanopore too fast to detect the changes in the current. The researchers slowed the DNA movement through the pore using a second protein called phi29 DNA polymerase (DNAP), which captures DNA and slows its movement through the pore.


The shape of the protein MspA meant that several bases passed through the nanopore at one time and the current changes were the result of a combination of those bases. This presented another challenge. Since several bases passed through the nanopore at one time, the researchers needed a way to decipher what the current changes meant. To do this, they first made a library of DNA sequences that contains all possible combinations of 4 nucleotides (for the mathematically inclined, the library is 44 = 256 bases long – a string of 4 bases with 4 possible choices for each DNA base). The library, whose sequence was already known, was run though the nanopore first to find the current associated with each set of DNA base combinations. They combined the library measurements with known genome sequences to generate a set of expected current changes that could be compared to experimental measurements.


The researchers tested their approach by sequencing the entire genome of bacteriophage Phi X 174, a virus that infects bacteria and is used as a benchmark for evaluating new sequencing technologies. The impressive feat here is the length of the genome they sequenced – the Phi X 174 genome is 4,500 bases long. Other nanopore technologies have been limited to sequencing DNA fragments that were much shorter.


“Despite the remaining hurdles, our demonstration that a low-cost device can reliably read the sequences of naturally occurring DNA and can interpret DNA segments as long as 4,500 nucleotides in length represents a major advance in nanopore DNA sequencing,” explained Gundlach.

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A Better Hand: Multitasking Like Never Before With These Robotic Fingers

A Better Hand: Multitasking Like Never Before With These Robotic Fingers | Amazing Science | Scoop.it

Many hands make light work, right? Well, MIT researchers have created a wrist-worn robot with a couple of extra digits.


There are several explanations for why the human hand developed the way it has. Some researchers link our opposable thumbs to our ancestors’ need to club and hurl objects at enemies or throw a punch, while others say that a unique gene enhancer (a group of proteins in DNA that activate certain genes) is what led to our anatomy. But most agree that bipedalism, enlarged brains and the need to use tools are what did the trick.


Yet, for as dexterous as our hands make us, a team of researchers at the Massachusetts Institute of Technology think we can do better. Harry Asada, a professor of engineering, has developed a wrist-worn robot that will allow a person to peel a banana or open a bottle one-handed


Together with graduate student Faye Wu, Asada built a pair of robotic fingers that track, mimic and assist a person’s own five digits. The two extra appendages, which look like elongated plastic pointer fingers, attach to a wrist cuff and extend alongside the thumb and pinkie. The apparatus connects to a sensor-laden glove, which measures how a person’s fingers bend and move. An algorithm crunches that movement data and translates it into actions for each robotic finger.


The robot takes a lesson from the way our own five digits move. One control signal from the brain activates groups of muscles in the hand. This synergy, Wu explains in a video demonstration, is much more efficient than sending signals to individual muscles.


In order to map how the extra fingers would move, Wu attached the device to her wrist and began grabbing objects throughout the lab. With each test, she manually positioned the robot fingers onto an object in a way that would be most helpful—for example, steadying a soda bottle while she used her hand to untwist the top. In each instance, she recorded the angles of both her own fingers and those of her robot counterpart.

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Single gene (Lhx1) found to control jet lag

Single gene (Lhx1) found to control jet lag | Amazing Science | Scoop.it

The discovery of the role of this gene, called Lhx1, provides scientists with a potential therapeutic target to help night-shift workers or jet lagged travelers adjust to time differences more quickly. The results, published in eLife, can point to treatment strategies for sleep problems caused by a variety of disorders.


“It’s possible that the severity of many dementias comes from sleep disturbances,” says Satchidananda Panda, a Salk associate professor who led the research team. “If we can restore normal sleep, we can address half of the problem.”


Every cell in the body has a “clock” – an abundance of proteins that dip or rise rhythmically over approximately 24 hours. The master clock responsible for establishing these cyclic circadian rhythms and keeping all the body’s cells in sync is the suprachiasmatic nucleus (SCN), a small, densely packed region of about 20,000 neurons housed in the brain’s hypothalamus.


More so than in other areas of the brain, the SCN’s neurons are in close and constant communication with one another. This close interaction, combined with exposure to light and darkness through vision circuits, keeps this master clock in sync and allows people to stay on essentially the same schedule every day. The tight coupling of these cells also helps make them collectively resistant to change. Exposure to light resets less than half of the SCN cells, resulting in long periods of jet lag.


In the new study, researchers disrupted the light-dark cycles in mice and compared changes in the expression of thousands of genes in the SCN with other mouse tissues. They identified 213 gene expression changes that were unique to the SCN and narrowed in on 13 of these that coded for molecules that turn on and off other genes. Of those, only one was suppressed in response to light: Lhx1.


“No one had ever imagined that Lhx1 might be so intricately involved in SCN function,” says Shubhroz Gill, a postdoctoral researcher and co-first author of the paper. Lhx1 is known for its role in neural development: it’s so important, that mice without the gene do not survive. But this is the first time it has been identified as a master regulator of light-dark cycle genes.

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Open access to the universe: Scientists generated a giant cosmic simulation and give it away for free

Open access to the universe: Scientists generated a giant cosmic simulation and give it away for free | Amazing Science | Scoop.it

A small team of astrophysicists and computer scientists have created some of the highest-resolution snapshots yet of a cyber version of our own cosmos. Called the Dark Sky Simulations, they’re among a handful of recent simulations that use more than 1 trillion virtual particles as stand-ins for all the dark matter that scientists think our universe contains.


They’re also the first trillion-particle simulations to be made publicly available, not only to other astrophysicists and cosmologists to use for their own research, but to everyone. The Dark Sky Simulations can now be accessed through a visualization program in coLaboratory, a newly announced tool created by Google and Project Jupyter that allows multiple people to analyze data at the same time.


To make such a giant simulation, the collaboration needed time on a supercomputer. Despite fierce competition, the group won 80 million computing hours on Oak Ridge National Laboratory’s Titan through the Department of Energy’s 2014 INCITE program.


In mid-April, the group turned Titan loose. For more than 33 hours, they used two-thirds of one of the world’s largest and fastest supercomputers to direct a trillion virtual particles to follow the laws of gravity as translated to computer code, set in a universe that expanded the way cosmologists believe ours has for the past 13.7 billion years.


“This simulation ran continuously for almost two days, and then it was done,” says Michael Warren, a scientist in the Theoretical Astrophysics Group at Los Alamos National Laboratory. Warren has been working on the code underlying the simulations for two decades. “I haven’t worked that hard since I was a grad student.”


Back in his grad school days, Warren says, simulations with millions of particles were considered cutting-edge. But as computing power has increased, particle counts did too. “They were doubling every 18 months. We essentially kept pace with Moore’s Law.”


When planning such a simulation, scientists make two primary choices: the volume of space to simulate and the number of particles to use. The more particles added to a given volume, the smaller the objects that can be simulated—but the more processing power needed to do it.


Current galaxy surveys such as the Dark Energy Survey are mapping out large volumes of space but also discovering small objects. The under-construction Large Synoptic Survey Telescope “will map half the sky and can detect a galaxy like our own up to 7 billion years in the past,” says Risa Wechsler, Skillman’s colleague at KIPAC who also worked on the simulation. “We wanted to create a simulation that a survey like LSST would be able to compare their observations against.”


The time the group was awarded on Titan made it possible for them to run something of a Goldilocks simulation, says Sam Skillman, a postdoctoral researcher with the Kavli Institute for Particle Astrophysics and Cosmology, a joint institute of Stanford and SLAC National Accelerator Laboratory. “We could model a very large volume of the universe, but still have enough resolution to follow the growth of clusters of galaxies.”


The end result of the mid-April run was 500 trillion bytes of simulation data. Then it was time for the team to fulfill the second half of their proposal: They had to give it away.

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Tracking the Ebola outbreak in near real-time: HealthMap, ProMED and other tools

Tracking the Ebola outbreak in near real-time: HealthMap, ProMED and other tools | Amazing Science | Scoop.it

Sobering news keeps coming out of the West African Ebola outbreak. According to numbers released on August 6, the virus has sickened 1,711 and claimed 932 lives across four nations. The outbreak continues to grow, with a high risk of continued regional spread, according to a threat analysis released byHealthMap (an outbreak tracking system operated out of Boston Children’s Hospital) and Bio.Diaspora (a Canadian project that monitors communicable disease spread via international travel).


“What we’ve seen here—because of inadequate public health measures, because of general fear—is [an outbreak that] truly hasn’t been kept under control,”John Brownstein, PhD, co-founder of HealthMap and a computational epidemiologist at Boston Children’s Hospital, told ABC News. “The event started, calmed down and jumped up again. Now, we’re seeing movement into densely populated areas, which is highly concerning.”


If you’re interested in keeping tabs on the outbreak yourself, there are several tools that can help:


  • HealthMap’s Ebola map. The HealthMap team is maintaining a dedicated, interactive map and timeline of the epidemic athealthmap.org/ebola (embedded at the top of this post). Both map and timeline are regularly updated as new information becomes available, as is the HealthMap Twitter account.
  • ProMED. The International Society for Infectious Disease, a non-profit organization for infectious and emerging disease research, operatesProMED, a disease news monitoring service that tracks outbreaks of human and veterinary infectious diseases. ProMED (short for Program for Monitoring Emerging Diseases) has been sending out regular email and Twitter alerts about the Ebola outbreak since it was first noticed in March.
  • US Centers for Disease Control and Prevention (CDC). The CDC is regularly posting updated news and patient counts—as well as travel and preparedness guidance and other information about the virus—on both their website and Twitter.
  • World Health Organization (WHO). The WHO’s Global Alert and Response system is providing regular updates on disease spread and control efforts. The organization is also distributing updates via its Twitter feed.
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Biodefense News's curator insight, August 14, 2014 10:20 PM

One glaring omission from this list is http://www.ascelbio.com, which is supplying CDC/GDD with outbreak information and forecasting.  Ascel Bio was also in constant contact with Samaritan's Purse and asked to help respond to evacuate.

Luigi Cappel's curator insight, August 16, 2014 5:53 PM

Not only is this a great site, but when I went in, it automatically identified that I live in New Zealand and showed me areas close to me where there are notifiable diseases. It showed that currently measles is growing around our country. This is a great site to check out, whether you are traveling overseas and want to see if there are things you want to be forewarned about, perhaps be inoculated against, or in the case of something like Ebola, places you might be better off staying well away from at least in the short to medium term. 

 

I recommend checking it out, whether you are traveling, or simply want to see great use of maps to show real time data. The time-lapse video showing the expansion of Ebola is fascinating. This is the sort of thing we usually just see on movies showing the CDC, like one of my favorite TV shows 24. Where's Jack Bauer when you need him? Oh, I here a rumor he may be coming back:)

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Flexible electronics: Fully printed organic thin film transistors (OTFTs) on a paper substrate

Flexible electronics: Fully printed organic thin film transistors (OTFTs) on a paper substrate | Amazing Science | Scoop.it
A nanoparticle ink that can be used for printing electronics without high-temperature annealing presents a possible profitable approach for manufacturing flexible electronics.


Printing semiconductor devices is considered to provide low-cost high performance flexible electronics that outperforms the amorphous silicon thin film transistors currently limiting developments in display technology. However the nanoparticle inks developed so far have required annealing, which limits them to substrates that can withstand high temperatures, ruling out a lot of the flexible plastics that could otherwise be used. Researchers at the National Institute for Materials Science and Okayama University in Japan have now developed a nanoparticle ink that can be used with room-temperature printing procedures.


Developments in thin film transistors made from amorphous silicon have provided wider, thinner displays with higher resolution and lower energy consumption. However further progress in this field is now limited by the low response to applied electric fields, that is, the low field-effect mobility. Oxide semiconductors such as InGaZnO (IGZO) offer better performance characteristics but require complicated fabrication procedures.


Nanoparticle inks should allow simple low-cost manufacture but the nanoparticles usually used are surrounded in non-conductive ligands – molecules that are introduced during synthesis for stabilizing the particles. These ligands must be removed by annealing to make the ink conducting. Takeo Minari, Masayuki Kanehara and colleagues found a way around this difficulty by developing nanoparticles surrounded by planar aromatic molecules that allow charge transfer.


The gold nanoparticles had a resistivity of around 9 x 10-6 Ω cm – similar to pure gold. The researchers used the nanoparticle ink to print organic thin film transistors on a flexible polymer and a paper substrate at room temperature, producing devices with mobilities of 7.9 and 2.5 cm2 V-1 s-1 for polymer and paper respectively – figures comparable to IGZO devices.


As the researchers conclude in their report of the work, "This room temperature printing process is a promising method as a core technology for future semiconductor devices."


Reference: Minari, T., Kanehara, Y., Liu, C., Sakamoto, K., Yasuda, T., Yaguchi, A., Tsukada, S., Kashizaki, K. and Kanehara, M. (2014), "Room-Temperature Printing of Organic Thin-Film Transistors with π-Junction Gold Nanoparticles." Adv. Funct. Mater.. doi: 10.1002/adfm.201400169

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Blood-brain-barrier disruption with high-frequency pulsed electric fields

Blood-brain-barrier disruption with high-frequency pulsed electric fields | Amazing Science | Scoop.it

A team of researchers from Virginia Tech and Wake Forest University School of Biomedical Engineering and Sciences have developed a new technique for using pulsed electric energy to open the blood-brain-barrier (BBB) for treating brain cancer and neurological disorders.

Their Vascular Enabled Integrated Nanosecond pulse (VEIN pulse) procedure consists of inserting minimally invasive needle electrodes into the diseased tissue and applying multiple bursts of 850-nanosecond pulsed electric energy with alternating polarity.


The researchers think the bursts disrupt tight junction proteins responsible for maintaining the integrity of the BBB, but without causing damage to the surrounding tissue. This technique will be described in the upcoming issue of the journal TECHNOLOGY.


For the treatment of brain cancer, “VEIN pulses could be applied at the same time as biopsy or through the same track as the biopsy probe in order to mitigate damage to the healthy tissue by limiting the number of needle insertions,” saysRafael V. Davalos, Ph.D, director of the Bioelectromechanical Systems Laboratory at Virginia Tech.


The BBB is a network of tight junctions that normally acts to protect the brain from foreign substances by preventing them from leaking from blood vessels into neural structures. But that also limits the effectiveness of drugs to treat brain disease. Temporarily opening the BBB is a way to ensure that drugs can still be effective.


Reference:
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Deadly Ebola Virus And The Development Of Designer Drugs To Fight The Disease

Deadly Ebola Virus And The Development Of Designer Drugs To Fight The Disease | Amazing Science | Scoop.it

The Ebola virus has sickened 1,711 people in West Africa and killed 932 in the latest outbreak, according to the World Health Organization. The virus has historically killed as many as 90 percent of those who contract it. The current outbreak has claimed the lives of about 60 percent of its victims.


On a small plot of land incongruously tucked amid a Kentucky industrial park sit five weather-beaten greenhouses. At the site, tobacco plants contain one of the most promising hopes for developing an effective treatment for the deadly Ebola virus.


The plants contain designer antibodies developed by San Diego-based Mapp Biopharmaceutical Inc. and are grown in Kentucky by a unit of Reynolds American Inc. Two stricken U.S. health workers received an experimental treatment containing the antibodies in Liberia last week. Since receiving doses of the drug, both patients’ conditions have improved.


Tobacco plant-derived medicines, which are also being developed by a company whose investors include Philip Morris International Inc., are part of a handful of cutting edge plant-based treatments that are in the works for everything from pandemic flu to rabies using plants such as lettuce, carrots and even duckweed. While the technique has existed for years, the treatments have only recently begun to reach the marketplace.


“Producing antibodies in plants is faster and less expensive than traditional manufacturing,” said Mary Kate Hart, an immunology researcher who did pioneering research on Ebola antibodies for the U.S. Army. She now is chief scientific officer for DynPort Vaccine Co.


Few modified-plant derived drugs have made it to market. Pfizer Inc. and Protalix Biotherapeutics Inc.’s enzyme Elelyso, produced in modified carrot cells was approved by U.S. regulators in 2012 to treat Gaucher’s disease. Locteron, an interferon-based hepatitis C drug candidate derived from duckweed, went through Phase 2 trials before its maker, Biolex Therapeutics Inc., declared bankruptcy. Neither drug is a monoclonal antibody and so far there has not been a vegetable-grown antibody approved by regulators, Chen said.


“Tobacco has always had negative press,” said Ebelhar, 66. “But now it may come back to be a benefit to mankind.’ Another tobacco giant-backed company working on biotech drugs grown in tobacco plants is Medicago Inc. in Quebec City, which is owned by Mitsubishi Tanabe Pharma Corp. and Philip Morris. Medicago is working on testing a vaccine for pandemic influenza and has a production greenhouse facility in North Carolina, said Jean-Luc Martre, senior director for government affairs at Medicago. Medicago is planning a final stage trial of the pandemic flu vaccine for next year, he said in a telephone interview. The plant method is flexible and capable of making antibodies and vaccines for numerous types of viruses, said Martre. In addition to influenza, the company’s website says it is in early stages of testing products for rabies and rotavirus.

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STAMP: Japanese universities develop new world's fastest camera

STAMP: Japanese universities develop new world's fastest camera | Amazing Science | Scoop.it

Researchers working at two universities in Japan have jointly developed what is being described as the world's fastest camera. A photo-device with a frame interval of 4.4 trillion frames per second. In their paper published in the journal Nature Photonics, the team describes how their camera works, its capabilities and the extensive work that went into its creation.


High speed cameras allow researchers and everyday people alike the ability to see things that they wouldn't be able to otherwise, from slowdown of sports play to mechanical processes. Prior to the announcement in Japan, the fastest cameras relied on what's known as a pump-probe process—where light is "pumped" at an object to be photographed, and then "probed" for absorption. The main drawback to such an approach is that it requires repetitive measurements to construct an image. The new camera is motion-based femtophotography, performing single-shot bursts for image acquisition, which means it has no need for repetitive measurements. It works via optical mapping of an object's spatial profile which varies over time. Its abilities make it 1000 times as fast as cameras it supersedes. In addition to the extremely high frame rate, the camera also has a high pixel resolution (450 × 450).


Developed by a joint team of researchers from Keio University and the University of Tokyo, the camera is set to capture images of things and events that until now have not been impossible. With technology the team has named Sequentially Timed All-optical Mapping Photography, or STAMP for short, the camera is poised to be used to capture chemical reactions, lattice vibrational waves, plasma dynamics, even heat conduction, which the researchers note occurs at approximately a sixth the speed that light travels.


The joint team has been working on development of the camera over the course of three years—plans call for continued development—the team would like to make the camera smaller (currently it's about a square meter) to allow for use in more applications. They also believe the camera could be used in a wide variety of fields, in both the public and private sectors. Some examples would be laser processes used for making big items like car parts, or in tiny applications such as the creation of semiconductors.


high-speed camera would allow researchers to actually see what is going on as the laser does its work. They also expect the camera to be useful in the medical field.

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NASA: Jupiter's Great Red Spot is Rapidly Shrinking

NASA: Jupiter's Great Red Spot is Rapidly Shrinking | Amazing Science | Scoop.it

New observations from the Hubble Space Telescope confirm that Jupiter's Great Red Spot is rapidly shrinking. The behemoth storm is now at its smallest size ever measured. According to Amy Simon of NASA's Goddard Space Flight Center in Greenbelt, Maryland, recent NASA Hubble Space Telescope observations confirm the Great Red Spot now is approximately 10,250 miles across, less than half the size of some historical measurements. Astronomers have followed this downsizing since the 1930s.


Historic observations as far back as the late 1800s gauged the storm to be as large as 25,500 miles on its long axis.  NASA Voyager 1 and Voyager 2 flybys of Jupiter in 1979 measured it to be 14,500 miles across. In 1995, a Hubble photo showed the long axis of the spot at an estimated 13,020 miles across. And in a 2009 photo, it was measured at 11,130 miles across. Beginning in 2012, amateur observations revealed a noticeable increase in the rate at which the spot is shrinking -- by 580 miles per year -- changing its shape from an oval to a circle.


"In our new observations it is apparent very small eddies are feeding into the storm," said Simon. "We hypothesized these may be responsible for the accelerated change by altering the internal dynamics and energy of the Great Red Spot."


Simon's team plans to study the motions of the small eddies and the internal dynamics of the storm to determine whether these eddies can feed or sap momentum entering the upwelling vortex, resulting in this yet unexplained shrinkage.


NASA's Juno spacecraft is hurtling toward Jupiter now, due to reach the giant planet in July 2016.  Point-blank examination by Juno's instruments will undoubtedly help unravel the mystery.


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New technique creates highly accurate detailed 3D maps in real time

New technique creates highly accurate detailed 3D maps in real time | Amazing Science | Scoop.it

Computer scientists at MIT and the National University of Ireland (NUI) at Maynooth have developed a mapping algorithm that creates dense, highly detailed 3-D maps of indoor and outdoor environments in real time.


The researchers tested their algorithm on videos taken with a low-cost Kinect camera, including one that explores the serpentine halls and stairways of MIT’s Stata Center. Applying their mapping technique to these videos, the researchers created rich, three-dimensional maps as the camera explored its surroundings.


As the camera circled back to its starting point, the researchers found that after returning to a location recognized as familiar, the algorithm was able to quickly stitch images together to effectively “close the loop,” creating a continuous, realistic 3-D map in real time.


The technique solves a major problem in the robotic mapping community that’s known as either “loop closure” or “drift”: As a camera pans across a room or travels down a corridor, it invariably introduces slight errors in the estimated path taken. A doorway may shift a bit to the right, or a wall may appear slightly taller than it is. Over relatively long distances, these errors can compound, resulting in a disjointed map, with walls and stairways that don’t exactly line up.


In contrast, the new mapping technique determines how to connect a map by tracking a camera’s pose, or position in space, throughout its route. When a camera returns to a place where it’s already been, the algorithm determines which points within the 3-D map to adjust, based on the camera’s previous poses.


“Before the map has been corrected, it’s sort of all tangled up in itself,” says Thomas Whelan, a PhD student at NUI. “We use knowledge of where the camera’s been to untangle it. The technique we developed allows you to shift the map, so it warps and bends into place.”


The technique, he says, may be used to guide robots through potentially hazardous or unknown environments. Whelan’s colleague John Leonard, a professor of mechanical engineering at MIT, also envisions a more benign application.

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Nikauly Vargas Arias's curator insight, August 14, 2014 4:44 PM

Interesante herramienta para la gestión sostenible del patrimonio construido

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Bert Vogelstein’s Liquid Biopsy Blood Test for DNA Could Stop Cancer in its Tracks

Bert Vogelstein’s Liquid Biopsy Blood Test for DNA Could Stop Cancer in its Tracks | Amazing Science | Scoop.it

He watched his brother die from a cancer that no drug could cure. Globally, eight million people died of cancer in 2012. Now one of the world’s most renowned cancer researchers says it’s time for Plan B. The answers Bert Vogelstein needed and feared were in the blood sample.


Vogelstein is among the most highly cited scientists in the world. He was described, in the 1980s, as having broken into “the cockpit of cancer” after he and coworkers at Johns Hopkins University showed for the first time exactly how a series of DNA mutations, adding up silently over decades, turn cells cancerous. Damaged DNA, he helped prove, is the cause of cancer.


Now imagine you could see these mutations—see cancer itself—in a vial of blood. Nearly every type of cancer sheds DNA into the bloodstream, and Vogelstein’s laboratory at Johns ­Hopkins has developed a technique, called a “liquid biopsy,” that can find the telltale genetic material.


The technology is made possible by instruments that speedily sequence DNA in a blood sample so researchers can spot tumor DNA even when it’s present in trace amounts. The ­Hopkins scientists, working alongside doctors who treat patients in Baltimore’s largest oncology center, have now studied blood from more than a thousand people. They say liquid biopsies can find cancer long before symptoms of the disease arise.


This particular blood sample, though, was personal. It was from Vogelstein’s brother, an orthopedic surgeon one year younger. He was fighting skin cancer, and the disease was already spreading. There was hope he’d respond to a new type of drug, but the treatment causes swelling, and it’s difficult to tell from an x-ray or CT scan whether the cancer is melting away or not. So Vogelstein used his lab’s new technology. If the cancer DNA had disappeared from the blood, they might celebrate. If it was still there, maybe he could steer his brother to some last-ditch drug.


“We tried to guide the treatment. That was the hope, anyway,” says Vogelstein. His voice tightens. He doesn’t say what happened next.

The obituary of Barry Vogelstein, born in Baltimore, appeared on July 3, 2013.


We’re not winning the war on cancer, and the death of ­Vogelstein’s brother shows why. Too many cancers are caught when they have become incurable. Each year, $91 billion is spent on cancer drugs worldwide, but most of those medicines are given to patients when it’s too late. The newest treatments, created at staggering expense, cost $10,000 a month and often extend life by only a few weeks. Pharmaceutical firms develop and test more drugs for late-stage cancer than for any other kind of disease.


“We as the public and as scientists have been entranced by this idea of curing advanced cancers,” says Vogelstein. “That is society’s Plan A. I don’t think that has to be the case.” There are other ways to reduce cancer deaths: wearing sunscreen, not smoking, and getting screened to catch cancer early. To ­Vogelstein, all these preventive steps represent “Plan B” because they receive so much less attention and funding. Yet when prevention works, it has better results than any drug. In the United States, the chance of dying from colorectal cancer is 40 percent lower than it was in 1975, a decrease mostly due to colonoscopy screening. Melanoma skin cancer, too, is treatable with surgery if caught early. “We think Plan B needs to be Plan A,” says Vogelstein.


The new blood tests could make that possible. For the first time, Hopkins researchers say, they are within reach of a general screening tool that could be used to scan broadly—perhaps at an annual physical—for molecular traces of cancer in people with no symptoms. “We think we’ve solved early detection,” says Victor Velculescu, a Hopkins researcher who runs a lab in the building next to Vogelstein’s.


Making such screening a routine practice in medicine will be challenging. One difficulty is that while the test may detect the presence of cancer DNA in the body, physicians might not know where the tumor is, how dangerous it is, or even whether it is worth treating. “We have to be cautious about how we talk about that,” says Daniel Haber, director of the Massachusetts General Hospital Cancer Center. He believes the DNA blood tests are “far from ready” and says very large studies will be needed to prove that they are useful. “There is a huge bar to get over,” he says.


Despite such skepticism, the technology is gaining attention. Tony Dickherber, head of the Innovative Molecular Analysis Technologies Program at the National Cancer Institute, says the idea of scanning blood for tumor DNA was “fringe at best” only three years ago. But now labs and companies from California to London are jumping in, producing a stream of improvements to the blood screening technology and new data supporting it. “People are starting to think that Vogelstein is right—this could be the best way to do early diagnosis,” he says. “[It] could be done much more widely than other screening technology we have, and you could screen for an incredible range of cancers.”

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AACR: Cancer Immunotherapy On Its Way To The Clinic

AACR: Cancer Immunotherapy On Its Way To The Clinic | Amazing Science | Scoop.it
Cancer immunotherapy refers to treatments that can unleash the power of a patient’s immune system to fight his or her cancer.


It seems that hardly a week goes by without there being a report of new breakthroughs in cancer immunotherapy. At the start of 2014, the focus was on the decision of the editors of Science to choose cancer immunotherapy as Breakthrough of the Year for 2013. In February, researchers at Memorial Sloan Kettering Cancer Center in New York published a study showing that 14 of 16 adults with relapsed or refractory acute lymphoblastic leukemia (ALL) had a complete response after treatment with an investigational cancer immunotherapy. And so it has gone on. Most recently, the U.S. Food and Drug Administration (FDA) granted breakthrough therapy designation to another investigational cancer immunotherapy, CTL019, for the treatment of pediatric and adult patients with relapsed/refractory ALL.


The excitement surrounding cancer immunotherapy was evident June 18, when a Twitter chat titled “The Promise of Immunotherapy,” organized by the American Association for Cancer Research (AACR) in partnership with Time magazine, the Mayo Clinic Cancer Center, and the Cancer Research Institute, reached an estimated 1.3 million individuals. But what is cancer immunotherapy, how does it work, and why are people so excited about it?


Cancer immunotherapy, which was featured as a key advance in patient care in the AACR Cancer Progress Report 2013, refers to treatments that can unleash the power of a patient’s immune system to fight his or her cancer. Decades of research have provided us with immense scientific insight into the immune system and how it interacts with cancer cells. This is what is allowing us to design increasing numbers of anticancer therapies that harness the immune system in different ways. It is also what is underpinning the groundswell of clinical trials testing cancer immunotherapies that we have seen in the past few years.


One of the reasons cancer immunotherapies have generated such excitement is that some have yielded dramatic and long-lasting responses in a number of patients. For example, Andrew Messinger (a cancer survivor featured in the AACR Cancer Progress Report 2013), who has metastatic melanoma – a disease that has an overall five-year survival rate of just 16 percent – is continuing to benefit from the cancer immunotherapy ipilimumab (Yervoy) five years after his first dose.


Ipilimumab is an example of a type of cancer immunotherapy known as a checkpoint inhibitor. These cancer immunotherapies work by releasing the ‘brakes’ on immune cells called T cells, which are naturally capable of destroying cancer cells. The brake released by ipilimumab is called CTLA4.


As highlighted in the AACR Cancer Progress Report 2014, which will be released in mid-September, a number of investigational cancer immunotherapies target a second T-cell brake called PD-1. One of these, pembrolizumab, is under review at the FDA as a potential treatment for metastatic melanoma. Another, nivolumab, received regulatory approval as a treatment for unresectable melanoma in Japan in July. Promising early results among patients with a number of other types of cancer, including non-small cell lung cancer and non-Hodgkin lymphoma, have been reported for PD-1-targeted cancer immunotherapies, but the data need to be confirmed in larger cohorts.


Despite all the excitement surrounding cancer immunotherapies, ipilimumab is one of the few currently approved by the FDA - it was approved for the treatment of metastatic melanoma in March 2011. As a result, most cancer immunotherapies remain investigational treatments, meaning that they have not yet been approved by the FDA and are still in development.


Fortunately, researchers are continuing to uncover new information about how the immune system functions. Thus, we can expect to see novel immunotherapies and new ways to use those that we already have in the future. Some of the most promising research in this area will be discussed at the AACR special conference Tumor Immunology and Immunotherapy: A New Chapter, which is being held in Orlando, Florida, Dec. 1-4. This conference is being put together in part by the AACR’s Cancer Immunology Working Group, which helps provide a forum for immunologists and non-immunologists to meet, exchange knowledge and ideas, and discuss the present status and future promise of cancer immunology.


Via Stefanie Charles
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Patient-Zero: Ebola outbreak probably started with a 2-year-old child in Guinea

Patient-Zero: Ebola outbreak probably started with a 2-year-old child in Guinea | Amazing Science | Scoop.it

he worst outbreak of Ebola, which has killed 961 people and triggered an international public health emergency, may have started with a 2-year-old patient in a village in Guinea.


About eight months ago, the toddler, whom researchers believe may have been Patient Zero, suffered fever, black stool and vomiting. Just four days after showing the painful symptoms, the child died on December 6, 2013, according to a report published in The New England Journal of Medicine.


Scientists don't know exactly how the toddler contracted the virus. Ebola is spread from animals to humans through infected fluids or tissue, according to the World Health Organization.


"In Africa, infection has been documented through the handling of infected chimpanzees, gorillas, fruit bats, monkeys, forest antelope and porcupines," WHO says, though researchers think fruit bats are what they call the virus's "natural host."


After the child's death, the mother suffered bleeding symptoms and died on December 13, according to the report. Then, the toddler's 3-year-old sister died on December 29, with symptoms including fever, vomiting and black diarrhea. The illness subsequently affected the toddler's grandmother, who died on January 1, in the family's village of Meliandou in Guéckédou.


The area in southern Guinea is close to the Sierra Leone and Liberia borders. The illness spread outside their village after several people attended the grandmother's funeral. Funerals tend to bring people in close contact with the body. Ebola spreads from person to person through contact with organs and bodily fluids such as blood, saliva, urine and other secretions of infected people. It has no known cure.

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Critical Immune System Control Mechanism Discovered

Critical Immune System Control Mechanism Discovered | Amazing Science | Scoop.it

Researchers at the Salk Institute say they have discovered a key control mechanism on regulatory T cells (Tregs) that determine if they send a halt signal to killer T cells during a pathogenic attack on the immune system. The new research (“Function of a Foxp3 cis-Element in Protecting Regulatory T Cell Identity”), published in Cell, could help develop treatments for autoimmune disorders as well as some types of cancer, according to the scientists.


When faced with pathogens, the immune system summons a swarm of cells made up of Tregs and killer T cells. Basically, Tregs tell killer T cells to halt “their attack” when invaders are cleared. Without this signal killer T cells continue their activities and turn on the body, causing inflammation and autoimmune disorders such as allergies, asthma, rheumatoid arthritis, multiple sclerosis, and type 1 diabetes.


“We discovered a mechanism responsible for stabilizing the cells that maintain immune system balance,” said senior author Ye Zheng, Salk Ph.D., assistant professor and holder of the Hearst Foundation Developmental Chair. “The immune system plays a huge role in chronic inflammation and if we can better understand the immune system, we can start to understand and treat many diseases.”


Tregs are like the surveillance system of the immune response, noted Dr. Zheng, adding that this surveillance system is “key to healthy immune reactions, but it can be kicked into overdrive or turned entirely off.”  For about a decade, researchers knew that the key to Tregs' peacekeeping ability was the Foxp3 gene, but they weren't sure how exactly it worked. Scientists also knew that under certain conditions, Tregs can go rogue: They transform into killer T cells and join in the immune system battle. This change means that they lose the ability to send a “halt” signal and add to inflammation.


In the new paper, Dr. Zheng's lab reports that a particular genetic sequence in Foxp3 is solely responsible for the stability of a Treg. If they removed the sequence, dubbed CNS2, Tregs became unstable and often morphed into killer T cells—the type of cell they are supposed to be controlling—resulting in autoimmune disease in animal models.


“Conserved noncoding sequence 2 (CNS2), a CpG-rich Foxp3 intronic cis-element specifically demethylated in mature Tregs, helps maintain immune homeostasis and limit autoimmune disease development by protecting Treg identity in response to signals that shape mature Treg functions and drive their initial differentiation,” wrote the researchers. “In activated Tregs, CNS2 helps protect Foxp3 expression from destabilizing cytokine conditions by sensing TCR/NFAT activation, which facilitates the interaction between CNS2 and Foxp3 promoter. Thus, epigenetically marked cis-elements can protect cell identity by sensing key environmental cues central to both cell identity formation and functional plasticity without interfering with initial cell differentiation.”

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Computer scientist reviews frontier technologies to determine fundamental limits of computer scaling

Computer scientist reviews frontier technologies to determine fundamental limits of computer scaling | Amazing Science | Scoop.it

From their origins in the 1940s as sequestered, room-sized machines designed for military and scientific use, computers have made a rapid march into the mainstream, radically transforming industry, commerce, entertainment and governance while shrinking to become ubiquitous handheld portals to the world.

This progress has been driven by the industry's ability to continually innovate techniques for packing increasing amounts of computational circuitry into smaller and denser microchips. But with miniature computer processors now containing millions of closely-packed transistor components of near atomic size, chip designers are facing both engineering and fundamental limits that have become barriers to the continued improvement of computer performance. Have we reached the limits to computation?


In a review article in this week's issue of the journal Nature, Igor Markov of the University of Michigan reviews limiting factors in the development of computing systems to help determine what is achievable, identifying "loose" limits and viable opportunities for advancements through the use of emerging technologies. His research for this project was funded in part by the National Science Foundation (NSF).


"Just as the second law of thermodynamics was inspired by the discovery of heat engines during the industrial revolution, we are poised to identify fundamental laws that could enunciate the limits of computation in the present information age," says Sankar Basu, a program director in NSF's Computer and Information Science and Engineering Directorate. "Markov's paper revolves around this important intellectual question of our time and briefly touches upon most threads of scientific work leading up to it."


The article summarizes and examines limitations in the areas of manufacturing and engineering, design and validation, power and heat, time and space, and information and computational complexity.


Via Jocelyn Stoller
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Researchers Develop Algorithm to Turn Erratic First-Person Footage Into Smooth Hyperlapse Videos

Researchers Develop Algorithm to Turn Erratic First-Person Footage Into Smooth Hyperlapse Videos | Amazing Science | Scoop.it

Three researchers at Microsoft Research (Johannes KopfMichael Cohen, and Richard Szeliski) have developed an algorithm that turns erratic first-person footage into smooth hyperlapse videos. The problem, as they put it, is that first-person footage is generally so long that the best way to actually view it is through a time-lapse video, but a time-lapse video further exacerbates the general shakiness and erratic nature of first-person footage. Kopf, Cohen, and Szeliski solve this problem through a complex algorithm that ultimately stitches and blends certain frames into a cohesive whole.


Our algorithm first reconstructs the 3D input camera path as well as dense, per-frame proxy geometries. We then optimize a novel camera path for the output video (shown in red) that is smooth and passes near the input cameras while ensuring that the virtual camera looks in directions that can be rendered well from the input.

More on the algorithm, including a more technical breakdown, is available at Microsoft Research.

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A self-organizing thousand-robot swarm can form any shape

A self-organizing thousand-robot swarm can form any shape | Amazing Science | Scoop.it

Following simple programmed rules, autonomous robots arrange themselves into vast, complex shapes.


“Form a sea star shape,” directs a computer scientist, sending the command to 1,024 little bots simultaneously via an infrared light. The robots begin to blink at one another and then gradually arrange themselves into a five-pointed star. “Now form the letter K.”


The ‘K’ stands for Kilobots, the name given to these extremely simple robots, each just a few centimeters across, standing on three pin-like legs. Instead of one highly-complex robot, a “kilo” of robots collaborate, providing a simple platform for the enactment of complex behaviors.


Just as trillions of individual cells can assemble into an intelligent organism, or a thousand starlings can form a great flowing murmuration across the sky, the Kilobots demonstrate how complexity can arise from very simple behaviors performed en masse (see video). To computer scientists, they also represent a significant milestone in the development of collective artificial intelligence (AI).


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RNA origami is a new method for self-organizing molecules on nanoscale

RNA origami is a new method for self-organizing molecules on nanoscale | Amazing Science | Scoop.it

Using just a single strand of RNA, many complicated shapes can be fabricated by RNA origami. Unlike existing methods for folding DNA molecules, RNA origamis are produced by enzymes and they simultaneously fold into pre-designed shapes. These features may allow designer RNA structures to be grown within living cells and used to organize cellular enzymes into biochemical factories. The method, which was developed by researchers from Aarhus University (Denmark) and California Institute of Technology, is reported in the latest issue of Science.


Origami, the Japanese art of paper folding, derives its elegance and beauty from the manipulation of a single piece of paper to make a complex shape. The RNA origami method described in the new study likewise involves the folding of a single strand of RNA, but instead of the experimenters doing the folding, the molecules fold up on their own.


"What is unique about the method is that the folding recipe is encoded into the molecule itself, through its sequence." explains Cody Geary, a postdoctoral scholar in the field of RNA structure and design at Aarhus University. "The sequence of the RNAs defines both the final shape and also the series of movements that rearrange the structures as they fold."


"The challenge of designing RNAs that fold up on their own is particularly difficult, since the molecules can easily get tangled during the folding process. So to design them, you really have to imagine the way that the molecules must twist and bend to obtain their final shape." Geary says.


The researchers used 3D models and computer software to design each RNA origami, which was then encoded as a synthetic DNA gene. Once the DNA gene was produced, simply adding the enzyme RNA-polymerase resulted in the automatic formation of RNA origami.


To observe the RNA molecules the researchers used an atomic force microscope, a type of scanning microscope that softly touches molecules instead of looking at them directly. The microscope is able to zoom in a thousand times smaller than is possible with a conventional light microscope. The researchers have demonstrated their method by folding RNA structures that form honeycomb shapes, but many other shapes should be realizable.


"We designed the RNA molecules to fold into honeycomb patterns because they are easy to recognize in the microscope. In one experiment we caught the polymerases in the process of making the RNAs that assemble into honeycombs, and they really look like honey bees in action." Geary continues.


A method for making origami shapes out of DNA has been around for almost a decade, and has since created many applications for molecular scaffolds. However, RNA has some important advantages over its chemical cousin DNA that make it an attractive alternative:


Paul Rothemund, a research professor at the California Institute of Technology and the inventor of the DNA origami method, is also an author on the new RNA origami work. "The parts for a DNA origami cannot easily be written into the genome of an organism. RNA origami, on the other hand, can be represented as a DNA gene, which in cells is transcribed into RNA by a protein machine called RNA polymerase." explains Rothemund.


Rothemund further adds, "The payoff is that unlike DNA origami, which are expensive and have to be made outside of cells, RNA origami should be able to be grown cheaply in large quantities, simply by growing bacteria with genes for them. Genes and bacteria cost essentially nothing to share, and so RNA origami will be easily exchanged between scientists."


The research was performed at laboratories at Aarhus University in Denmark, and the California Institute of Technology in Pasadena. Ebbe Andersen, an Assistant Professor at Aarhus University, who works on developing molecular biosensors, lead the development of the project.


"All of the molecules and structures that form inside of living cells are the products of self-assembly, but we still know very little about how self-assembly actually works. By designing and testing self-assembling RNA shapes, we have begun to shed some light on fundamental principles of self-assembly." says Andersen.

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Eco-friendly ‘pre-fab’ self-assembling nanoparticles could revolutionize nano manufacturing

Eco-friendly ‘pre-fab’ self-assembling nanoparticles could revolutionize nano manufacturing | Amazing Science | Scoop.it

University of Massachusetts Amherst scientists have developed a breakthrough technique for creating water-soluble nano-modules and controlling molecular assembly of nanoparticles over multiple length scales.


The new method should reduce the time nanotech manufacturing firms spend in trial-and-error searches for materials to make electronic devices such as solar cells, organic transistors, and organic light-emitting diodes.


“The old way can take years,” says materials chemist Paul Lahti, co-director with Thomas Russell of UMass Amherst’s Energy Frontiers Research Center (EFRC), supported by the U.S. Department of Energy.


“Another of our main objectives is to make something that can be scaled up from nano- to mesoscale, and our method does that. It is also much more ecologically friendly because we use water instead of dangerous solvents in the process.


“In our recent paper, we worked on glass, but we want to translate to flexible materials and produce roll-to-roll manufactured materials with water,” said chemist Dhandapani Venkataraman, lead investigator. “We expect to actually get much greater efficiency.” He suggests that reaching 5 percent power conversion efficiency would justify the investment for making small, flexible solar panels to power devices such as smart phones.


If the average smart phone uses 5 watts of power and all 307 million United States users switched from batteries to flexible solar, it could save more than 1500 megawatts per year, Venkataraman estimates. “That’s nearly the output of a nuclear power station,” he says, “and it’s more dramatic when you consider that coal-fired power plants generate 1 megawatt and release 2,250 lbs. of carbon dioxide. So if a fraction of the 6.6 billion mobile phone users globally changed to solar, it would reduce our carbon footprint a lot.”


Doctoral student and first author Tim Gehan says that organic solar cells made in this way can be semi-transparent, as well, “so you could replace tinted windows in a skyscraper and have them all producing electricity during the day when it’s needed. And processing is much cheaper and cleaner with our cells than in traditional methods.”

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Computer generated math proof is too large for humans to check

Computer generated math proof is too large for humans to check | Amazing Science | Scoop.it

A pair of mathematicians, Alexei Lisitsa and Boris Konev of the University of Liverpool, U.K., have come up with an interesting problem—if a computer produces a proof of a math problem that is too big to study, can it be judged as true anyway? In a paper they've uploaded to the preprint server arXiv, the two describe how they set a computer program to proving a small part of what's known as "Erdős discrepancy problem"—the proof produced a data file that was 13-gigabytes in size—far too large for any human to check, leading to questions as to whether the proof can be taken as a real proof.

Anyone who has taken a high level math course can attest to the fact that math proofs can sometimes grow long—very long. Some mathematicians have dedicated years to creating them, filling whole text volumes in the process. Quite naturally then, mathematicians have increasingly turned to computers to perform some of the more mundane parts of proof creation. It wasn't long, however, before some began to realize that at some point, the proofs spit out by the computer would be too long, complicated or both for a human reader to fully comprehend. It appears, with this new effort that that day might have come.


Erdős discrepancy problem revolves around trying to find patterns in an infinite list of just the two numbers "1" and "-1". Named after Paul Erdős, the discrepancy problem arises when cutting off the infinite sequence at some point and then creating a finite sequence using a defined constant. When the numbers are added up, the result is called the discrepancy figure. Lisitsa and Konev entered the problem (with a discrepancy constant of 2) into a computer running what they describe as state of the art SAT solvers—software that has been written to create mathematical proofs. The proof that the computer came up with proves, the two researchers claim, "that no sequence of length 1161 and discrepancy 2 exists."


Unfortunately the file produced was too large to read—for comparison's sake, it was a couple of gigabytes larger than the whole of Wikipedia. This leads to an interesting conundrum for mathematicians going forward.


Do we begin accepting proofs that computers create as actual proofs if they are too long or perhaps too difficult for our minds to comprehend? If so, we might just be at a crossroads. Do we trust computers to handle things for us that our beyond our abilities, or constrain our reach by refusing to allow for the creation of things that we cannot ever possibly understand?

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A possible signal from dark matter?

A possible signal from dark matter? | Amazing Science | Scoop.it

Galaxies are often found in groups or clusters, the largest known aggregations of matter and dark matter. The Milky Way, for example, is a member of the "Local Group" of about three dozen galaxies, including the Andromeda Galaxy located about 2 million light-years away. Very large clusters can contain thousands of galaxies, all bound together by gravity. The closest large cluster of galaxies to us, the Virgo Cluster with about 2000 members, is about 50 million light-years away. The Perseus Cluster is one of the most massive objects in the Universe with thousands of galaxies immersed in an enormous cloud of superheated gas.


The space between galaxies is not empty. It is filled with hot intergalactic gas whose temperature is of order ten million kelvin, or even higher. The gas is enriched with heavy elements that escape from the galaxies and accumulate in the intracluster medium over billions of years of galactic and stellar evolution. These intracluster gas elements can be detected from their emission lines in X-ray, and include oxygen, neon, magnesium, silicon, sulfur, argon, calcium, iron, nickel, and even chromium and manganese.


The relative abundances of these elements contain valuable information on the rate of supernovae in the different types of galaxies in the clusters since supernovae make and/or disburse them into the gas. Therefore it came as something of a surprise when CfA astronomers and their colleagues discovered a faint line corresponding to no known element. Esra Bulbul, Adam Foster, Randall Smith, Scott Randall and their team were studying the averaged X-ray spectrum of a set of seventy-three clusters (including Virgo) looking for emission lines too faint to be seen in any single one when they uncovered a line with no known match in a particular spectral interval not expected to have any features.


The scientists propose a tantalizing suggestion: the line is the result of the decay of a putative, long-sought-after dark matter particle, the so-called sterile neutrino. It had been suggested that the hot X-ray emitting gas in a galaxy cluster might be a good place to look for dark matter signatures, and if the sterile neutrino result is confirmed it would mark a breakthrough in dark matter research (it is of course possible that it is a statistical or other error). Recent unpublished results from another group tend to support the detection of this feature; the team suggests that observations with the planned Japanese Astro-H X-ray mission in 2015 will be critical to confirm and resolve the nature of this line.


More information: "Detection of an Unidentified Emission Line in the Stacked X-Ray Spectrum of Galaxy Clusters," Esra Bulbul, Maxim Markevitch, Adam Foster, Randall K. Smith, Michael Loewenstein, and Scott W. Randall, ApJ 789, 13, 2014.

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Gene that controls nerve conduction velocity linked to multiple sclerosis.

Gene that controls nerve conduction velocity linked to multiple sclerosis. | Amazing Science | Scoop.it

A new study from the University of Lubeck identifies a novel gene that controls nerve conduction velocity. Investigators report that even minor reductions in conduction velocity may aggravate disease in multiple sclerosis (MS) patients and in mice bred for the MS-like condition experimental autoimmune encephalomyelitis (EAE).


A strong tool for investigating the pathophysiology of a complex disease is the identification of underlying genetic controls. Multiple genes have been implicated as contributing to the risk of developing MS. Unlike studies that have focused on genetic regulators of inflammation, autoimmunity, demyelination, and neurodegeneration in MS, this study focused on nerve conduction velocity. Investigators found that polymorphisms of the inositol polyphosphate-4-phosphatase, type II (Inpp4b) gene affect the speed of nerve conduction in both mice with EAE and humans with MS.


Impairment of nerve conduction is a common feature in neurodegenerative and neuroinflammatory diseases such as MS. Measurement of evoked potentials (whether visual, motor, or sensory) is widely used for diagnosis and recently also as a prognostic marker for MS.


Using several genomic approaches, the investigators narrowed their search to the genetic region controlling the enzyme inositol-polyphosphate-4-phosphatase II (INPP4B), the product of which helps to regulate the phosphatidyl inositol signaling pathway. Enzymes in this family are involved in cellular functions such as cell growth, proliferation, differentiation, motility, survival, and intracellular communication.


In one series of experiments, the researchers analyzed the genetic locus EAE31, which previously had been shown to control the latency of motor evoked potentials and clinical onset of EAE in mice. Using advanced techniques including congenic mapping, in silico haplotype analyses (computer simulations), and comparative genomics (from rats, mice and humans), they were able to ‘finemap’ the focus to Inpp4b as the quantitative trait gene for EAE31.


When the investigators analyzed this region in eight different strains of mice, they found they could divide the strains into two groups based on differences in amino acid sequences. The strains with the longer-latency SJL/J allele had the two amino acids (arginine and proline), whereas those with the shorter-latency C57BL/10S allele had others (serine and histidine).  These data suggest that Inpp4b structural polymorphism is associated with the speed of neuronal conduction.


In another experiment, the scientists compared motor conduction velocity in genetically modified mice with a mutant Inpp4b gene to that of control mice. The nerve conduction in this group was slower than in the control group.


Finally, the investigators studied INPP4B polymorphisms in MS patients. They looked at two cohorts: one from Spain (349 cases and 362 controls) and a second from Germany (562 cases and 3,314 controls). The association between the INPP4B polymorphisms and susceptibility to MS was statistically significant when the cohorts were pooled.


However, although the Spanish cohort showed a strong association between INPP4B and MS, the association was weaker in the German cohort. The exact reason for the diverging effect across these populations remains unresolved.

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CurvACE gives robots a bug’s eye view

CurvACE gives robots a bug’s eye view | Amazing Science | Scoop.it

The vertebrate eye has provided inspiration for the design of conventional cameras with single-aperture optics to provide a faithful rendering of the visual world. The insect compound eye, in spite of bearing a comparatively lower resolution than the vertebrate eye, is very efficient for local and global motion analysis over a large field of view (FOV), making it an excellent sensor for accurate and fast navigation in 3D dynamic environments. Furthermore, compound eyes take several shapes and curvatures to fit the head and viewing directions of very different types of insects while offering the same functionality.


The goal of this project is to design, develop, and assess a novel curved and flexible vision sensor for fast extraction of motion-related information. These integrated systems are called CURVed Artificial Compound Eyes (CURVACE). Compared to conventional cameras, artificial compound eyes will offer more efficient visual abilities for motion analysis,  a much larger field of view in a smaller size and weight, bearing a thin packaging and being self-contained and programmable.


Additionally, the CURVACE developers will use neuromorphic imagers with adaptive sensitivity, and the rendered images will yield less distortion and less aberration. The fabricated CURVACE will bear mechanical adaptability to a range of shapes and curvatures, and some versions will offer space within the convexity for embedding processing units, battery, or additional sensors that are useful for motion-related computation.


The findings of the CurvACE project were published in PNAS.

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Mouse Avatars: Personalized Cancer Grafting Offers Clues to Individualized Treatment

Mouse Avatars: Personalized Cancer Grafting Offers Clues to Individualized Treatment | Amazing Science | Scoop.it

For $12,000, a company grafts a patient’s cancer into rodents and tests drugs on them. At a laboratory in Baltimore, hairless mice kept in racks of plastic crates are labelled with yellow cards, each identifying a person fighting cancer. These mice are cancer “avatars”—the lumpy tumors visible under their skin come from actual patients.


The technology is a twist on personalized medicine that’s being developed by Champions Oncology. The company, based in New Jersey and Maryland, has started offering mouse avatars directly to patients, at a cost of $10,000 to $12,000. Insurance companies don’t yet pay for the technology, which remains experimental.


In the service Champions is selling, doctors first remove a piece of a patient’s tumor during a surgery or biopsy. Then they ship it to the company, where it gets grafted under the skin of an immune-deficient mouse. Because the rodents have impaired defenses, the human tumor is able to grow. Parts of it can be removed and implanted in additional mice.


The data from the avatars is potentially life-saving, since the choice of what drug to give a cancer patient is often made by guesswork or trial and error. “Generally, the drugs we give to patients are more likely to not work than to work,” says Justin Stebbing, an oncologist at the Imperial College London, who has been involved in medical studies of Champions’s technology. The results from the personalized mice, he says, “give patients an additional layer of confidence.”


Cancer avatars are part of a wider effort to carry out experiments on people’s tumors outside their bodies. Some researchers have created fruit flies that share the same gene mutations patients have. Another technology, still in development, looks to capture floating tumor cells from a person’s bloodstream, then grow and test them in culture dishes (see “A Laboratory for Rare Cells Sheds Light on Cancer”). Still further out, scientists have plans to grow mini-organs, complete with an immune system that matches the patient’s (see “Building an Organ on a Chip”).


Over the last few decades, study of cancer in mouse models has gained popularity. Sophisticated genetic manipulation technologies and commercialization of these murine systems have made it possible to generate mice to study human disease. Given the large socio-economic burden of cancer, both on academic research and the health care industry, there is a need for in vivo animal cancer models that can provide a rationale that is translatable to the clinic. Such a bench-to-bedside transition will facilitate a long term robust strategy that is economically feasible and clinically effective to manage cancer. The major hurdles in considering mouse models as a translational platform are the lack of tumor heterogeneity and genetic diversity, which are a hallmark of human cancers. The present review, while critical of these pitfalls, discusses two newly emerging concepts of personalized mouse models called “Mouse Avatars” and Co-clinical Trials. Development of “Mouse Avatars” entails implantation of patient tumor samples in mice for subsequent use in drug efficacy studies. These avatars allow for each patient to have their own tumor growing in an in vivo system, thereby allowing the identification of a personalized therapeutic regimen, eliminating the cost and toxicity associated with non-targeted chemotherapeutic measures. In Co-clinical Trials, genetically engineered mouse models (GEMMs) are used to guide therapy in an ongoing human patient trial. Murine and patient trials are conducted concurrently, and information obtained from the murine system is applied towards future clinical management of the patient’s tumor. The concurrent trials allow for a real-time integration of the murine and human tumor data. In combination with several molecular profiling techniques, the “Mouse Avatar” and Co-clinical Trial concepts have the potential to revolutionize the drug development and health care process.

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