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Take a swab of saliva from your mouth and within minutes your DNA could be ready for analysis and genome sequencing with the help of a new device. University of Washington engineers and NanoFacture, a Bellevue, Wash., company, have created a device that can extract human DNA from fluid samples in a simpler, more efficient and environmentally friendly way than conventional methods. The device will give hospitals and research labs a much easier way to separate DNA from human fluid samples, which will help with genome sequencing, disease diagnosis and forensic investigations. “It’s very complex to extract DNA,” said Jae-Hyun Chung, a UW associate professor of mechanical engineering who led the research. “When you think of the current procedure, the equivalent is like collecting human hairs using a construction crane.” This technology aims to clear those hurdles. The small, box-shaped kit now is ready for manufacturing, then eventual distribution to hospitals and clinics. NanoFacture, a UW spinout company, signed a contract with Korean manufacturer KNR Systems last month at aceremony in Olympia, Wash. The UW, led by Chung, spearheaded the research and invention of the technology, and still manages the intellectual property. Separating DNA from bodily fluids is a cumbersome process that’s become a bottleneck as scientists make advances in genome sequencing, particularly for disease prevention and treatment. The market for DNA preparation alone is about $3 billion each year. Conventional methods use a centrifuge to spin and separate DNA molecules or strain them from a fluid sample with a micro-filter, but these processes take 20 to 30 minutes to complete and can require excessive toxic chemicals. UW engineers designed microscopic probes that dip into a fluid sample – saliva, sputum or blood – and apply an electric field within the liquid. That draws particles to concentrate around the surface of the tiny probe. Larger particles hit the tip and swerve away, but DNA-sized molecules stick to the probe and are trapped on the surface. It takes two or three minutes to separate and purify DNA using this technology.
Researchers at Brown University have succeeded in creating the first wireless, implantable, rechargeable, long-term brain-computer interface. The wireless BCIs have been implanted in pigs and monkeys for over 13 months without issue, and human subjects are next. A tether limits the mobility of the patient, and also the real-world testing that can be performed by the researchers. Brown’s wireless BCI allows the subject to move freely, dramatically increasing the quantity and quality of data that can be gathered — instead of watching what happens when a monkey moves its arm, scientists can now analyze its brain activity during complex activity, such as foraging or social interaction. Obviously, once the wireless implant is approved for human testing, being able to move freely — rather than strapped to a chair in the lab — would be rather empowering. Inside the device, there’s a li-ion battery, an inductive (wireless) charging loop, a chip that digitizes the signals from your brain, and an antenna for transmitting those neural spikes to a nearby computer. The BCI is connected to a small chip with 100 electrodes protruding from it, which, in this study, was embedded in the somatosensory cortex or motor cortex. These 100 electrodes produce a lot of data, which the BCI transmits at 24Mbps over the 3.2 and 3.8GHz bands to a receiver that is one meter away. The BCI’s battery takes two hours to charge via wireless inductive charging, and then has enough juice to last for six hours of use.
One of the features that the Brown researchers seem most excited about is the device’s power consumption, which is just 100 milliwatts. For a device that might eventually find its way into humans, frugal power consumption is a key factor that will enable all-day, highly mobile usage. Amusingly, though, the research paper notes that the wireless charging does cause significant warming of the device, which was “mitigated by liquid cooling the area with chilled water during the recharge process and did not notably affect the animal’s comfort.” Another important factor is that the researchers were able to extract high-quality, “rich” neural signals from the wireless implant — a good indicator that it will also help human neuroscience, if and when the device is approved.
German and Hungarian researchers have brought sight to nine blind patients with hereditary retinal degeneration, using a subretinally implanted microelectronic chip with 1500 pixels. The chip size is approximately 3mm x 3mm and is surgically implanted below the fovea (area of sharpest vision in the retina). It provides a diamond-shaped visual field of 15 degrees diagonally across chip corners. It is powered by a subdermal coil behind the ear that is powered from a battery via transdermal inductive transmission. The core of the implant is a microchip with 1,500 pixels, each 70 x 70 microns. Photocells, an amplifying circuit, and a stimulation electrode are attached to each pixel. The photocells absorb the light entering the eye, transforming it into electrical signals. A tiny power line provides energy from the subdermal coil Sixteen additional electrodes are placed for testing purposes at the tip of the implant. The incoming light intensity controls the amount of current released by each electrode, stimulating the neighboring intact retinal nerve cells electrically. The nerve impulses generated by the retinal cells are processed in the remaining neuronal network of the retina and transmitted via the optic nerve to the visual cortex, creating visual sensations. An unimpaired, regularly functioning optic nerve is required.
“So far, our approach using subretinal electronic implants is the only one that has successfully mediated images in a trial with freely moving blind persons by means of a light sensor array that moves with the eye,” the scientists said. “All the other current approaches require an extraocular camera that does not link image capture to eye movements, which, therefore, does not allow the utilization of microsaccades for refreshing the perceived images.” In most hereditary retinal diseases, such as retinitis pigmentosa, the photoreceptors progressively degenerate, often causing blindness in adult life, and there is no therapy available to treat this disease.
IBM's Watson—the same machine that beat Ken Jennings at Jeopardy—is now churning through case histories at Memorial Sloan-Kettering, learning to make diagnoses and treatment recommendations. This is one in a series of developments suggesting that technology may be about to disrupt health care in the same way it has disrupted so many other industries. “n Brazil and India, machines are already starting to do primary care, because there’s no labor to do it. They may be better than doctors. Mathematically, they will follow evidence—and they’re much more likely to be right. Harley Lukov didn’t need a miracle. He just needed the right diagnosis. Lukov, a 62-year-old from central New Jersey, had stopped smoking 10 years earlier—fulfilling a promise he’d made to his daughter, after she gave birth to his first grandchild. But decades of cigarettes had taken their toll. Lukov had adenocarcinoma, a common cancer of the lung, and it had spread to his liver. The oncologist ordered a biopsy, testing a surgically removed sample of the tumor to search for particular “driver” mutations. A driver mutation is a specific genetic defect that causes cells to reproduce uncontrollably, interfering with bodily functions and devouring organs. Think of an on/off switch stuck in the “on” direction. With lung cancer, doctors typically test for mutations called EGFR and ALK, in part because those two respond well to specially targeted treatments. But the tests are a long shot: although EGFR and ALK are the two driver mutations doctors typically see with lung cancer, even they are relatively uncommon. When Lukov’s cancer tested negative for both, the oncologist prepared to start a standard chemotherapy regimen—even though it meant the side effects would be worse and the prospects of success slimmer than might be expected using a targeted agent. But Lukov’s true medical condition wasn’t quite so grim. The tumor did have a driver—a third mutation few oncologists test for in this type of case. It’s called KRAS. Researchers have known about KRAS for a long time, but only recently have they realized that it can be the driver mutation in metastatic lung cancer—and that, in those cases, it responds to the same drugs that turn it off in other tumors. A doctor familiar with both Lukov’s specific medical history and the very latest research might know to make the connection—to add one more biomarker test, for KRAS, and then to find a clinical trial testing the efficacy of KRAS treatments on lung cancer. But the national treatment guidelines for lung cancer don’t recommend such action, and few physicians, however conscientious, would think to do these things. Did Lukov ultimately get the right treatment? Did his oncologist make the connection between KRAS and his condition, and order the test? He might have, if Lukov were a real patient and the oncologist were a real doctor. They’re not. They are fictional composites developed by researchers at the Memorial Sloan-Kettering Cancer Center in New York, in order to help train—and demonstrate the skills of—IBM’s Watson supercomputer. Yes, this is the same Watson that famously went on Jeopardy and beat two previous human champions. But IBM didn’t build Watson to win game shows. The company is developing Watson to help professionals with complex decision making, like the kind that occurs in oncologists’ offices—and to point out clinical nuances that health professionals might miss on their own. Watson has gotten some media hype already, including articles in Wired and Fast Company. Still, you probably shouldn’t expect to see it the next time you visit your doctor’s office. Before the computer can make real-life clinical recommendations, it must learn to understand and analyze medical information, just as it once learned to ask the right questions on Jeopardy. That’s where Memorial Sloan-Kettering comes in. The famed cancer institute has signed up to be Watson’s tutor, feeding it clinical information extracted from real cases and then teaching it how to make sense of the data. “The process of pulling out two key facts from aJeopardy clue is totally different from pulling out all the relevant information, and its relationships, from a medical case,” says Ari Caroline, Sloan-Kettering’s director of quantitative analysis and strategic initiatives. “Sometimes there is conflicting information. People phrase things different ways.” But Caroline, who approached IBM about the research collaboration, nonetheless predicts that Watson will prove “very valuable”—particularly in a field like cancer treatment, in which the explosion of knowledge is already overwhelming. “If you’re looking down the road, there are going to be many more clinical options, many more subtleties around biomarkers … There will be nuances not just in interpreting the case but also in treating the case,” Caroline says. “You’re going to need a tool like Watson because the complexity and scale of information will be such that a typical decision tool couldn’t possibly handle it all.” The Cleveland Clinic is also helping to develop Watson, first as a tool for training young physicians and then, possibly, as a tool at the bedside itself. James Young, the executive dean of the Cleveland Clinic medical school, told The Plain Dealer, “If we can get Watson to give us information in the health-care arena like we’ve seen with more-general sorts of knowledge information, I think it’s going to be an extraordinary tool for clinicians and a huge advancement.” And WellPoint, the insurance company, has already begun testing Watson as a support tool for nurses who make treatment-approval decisions. Whether these experiments show real, quantifiable improvements in the quality or efficiency of care remains to be seen. If Watson tells physicians only what they already know, or if they end up ordering many more tests for no good reason, Watson could turn out to be more hindrance than help. But plenty of serious people in the fields of medicine, engineering, and business think Watson will work (IBM says that it could be widely available within a few years). And many of these same people believe that this is only the beginning—that whether or not Watson itself succeeds, it is emblematic of a quantum shift in health care that’s just now getting under way.
If engineers at Stanford have their way, biological research may soon be transformed by a new class of light-emitting probes small enough to be injected into individual cells without harm to the host. Welcome to biophotonics, a discipline at the confluence of engineering, biology and medicine in which light-based devices – lasers and light-emitting diodes (LEDs) – are opening up new avenues in the study and influence of living cells. The team described their probe in a paper published online Feb. 13, 2013 by the journal Nano Letters. It is the first study to demonstrate that tiny, sophisticated devices known as light resonators can be inserted inside cells without damaging the cell. Even with a resonator embedded inside, a cell is able to function, migrate and reproduce as normal. The researchers call their device a "nanobeam," because it resembles a steel I-beam with a series of round holes etched through the center. This beam, however, is not massive, but measure only a few microns in length and just a few hundred nanometers in width and thickness. It looks a bit like a piece from an erector set of old. The holes through the beam act like a nanoscale hall of mirrors, focusing and amplifying light at the center of the beam in what are known as photonic cavities.
Structurally, the new device is a sandwich of extremely thin layers of the semiconductor gallium arsenide alternated with similarly thin layers of light-emitting crystal, a sort of photonic fuel known as quantum dots. The structure is carved out of chips or wafers, much like sculptures are chiseled out of rock. Once sculpted, the devices remain tethered to the thick substrate. For biological applications, the thick, heavy substrate presents a serious hurdle for interfacing with single cells. The underlying and all-important nanocavities are locked in position on the rigid material and unable to penetrate cell walls. Shambat's breakthrough came when he was able to peel away the photonic nanobeams. He then glued the ultrathin photonic device to a fiberoptic cable with which he steers the needle-like probe toward and into the cell.
Once inserted in the cell, the probe emits light, which can be observed from outside. For engineers, it means that almost any application of these powerful photonic devices can be translated into the previously off-limits environment of the cell interior. In one finding that the authors describe as stunning, they loaded their nanobeams into cells and watched as the cells grew, migrated around the research environment and reproduced. Each time a cell divided, one of the daughter cells inherited the nanobeam from the parent and the beam continued to function as expected. This inheritability frees researchers to study living cells over long periods of time, a research advantage not possible with existing detection techniques, which require cells be either dead or fixed in place. "Our nanoscale probes can reside in cells for long periods of time, potentially providing sensor feedback or giving control signals to the cells down the road," said Shambat. "We tracked one cell for eight days. That's a long time for a single-cell study."
For the first time, Wayne State University researchers have shown brain connectivity in fetuses, a discovery that could lead to new ways to prevent and treat brain disorders. Research has shown that brain disorders such as autism may begin in fetal life but there hasn't been a method for seeing and studying brain development at that stage. But Thomason's study showed that the fetal brain can be studied while in the womb using MRI scans that do not threaten the health of the infant or mother, providing a mechanism for many researchers to study fetal brain connections as they are forming and possibly learn how a lack of connections can result in brain disorders. "By understanding how a lack of (brain) connectivity occurs, the research community can begin to identify what things influence early brain development," Thomason said. "If we know what disrupts or impedes healthy brain development, then we have a better shot at finding a way to treat and possibly prevent it." The research, which began in November, was funded partly by the NIH and WSU. It included 25 fetuses between 24 to 38 weeks of gestation. The findings show that brain connections strengthened between the right and left side as fetuses developed and short-distance connections in the brain network are more strongly connected than long-range connections. It is the first study of a larger project that seeks to define how functional brain networks form in fetuses and examine the environment of the developing child in utero, and factors in the mother's life. The project plans to track the fetuses once they become infants and throughout their life so researchers can compare their neurodevelopment to what was seen in the womb. The hope is to even study the children of these fetuses, if funding allows.
In 1993, scientists working for pharmaceutical giant Pfizer had a conundrum on their hands. Their new wonder drug, the product of years of intense and costly research, failed to show any effectiveness in treating patients with angina pectoris, a common cause of severe chest pain. Then named UK-92,480, the drug was destined to be shelved. if it were not for the keen observation that some patients reported sustained erections as a side effect of their treatment. The researchers were baffled at first but then realized the opportunity on their hands. Five years later, UK-92,480 gained FDA approval as an oral treatment for erectile dysfunction and was released to market. Today it has been rebranded as sildenafil — or Viagra — and has become a windfall for Pfizer. Could other failed drugs find their own stories of serendipity? Certainly, finding novel uses for failed drugs is not a new idea. Aside from Viagra, a number of well-known drugs had originally been developed for other purposes, such as Rogaine, which had started as a drug for high blood pressure, and AZT, the anti-HIV drug that was originally supposed to be a cancer drug. In each case, advances in our understanding of diseases and human biology led researchers back to the past, repurposing old drugs based on a better understanding of their mechanisms of action. Pharmaceutical companies have taken an interest in reviving their failed drugs. From their perspective, drug development is a risky business. Bringing a drug from the lab to the clinic typically takes 13 years and an investment of around $1 billion, with a 95 percent risk of failure. Some drugs may not be structurally suitable for efficient mass production, some show dangerous side effects, and some simply do not work against the target disease. In total, around 30,000 drugs have been shelved by pharmaceutical companies over the past three decades, and some of these failed drugs have shown new promise for treating other diseases. Because they have already been tested in humans, details about their production, dosage, and toxicity are readily available, which can expedite the process of developing new disease treatments. Instead of starting from scratch, successful repurposing of even a few drugs could save companies substantial amounts of cost and time. A new development in drug retargeting strategies has been the creation of drug libraries that allow receptor sites to be matched up with pre-existing chemical compounds. Last year, Dr. Elias Lolis, Professor of Pharmacology at Yale School of Medicine, and Dr. Michael Cappello, Professor of Pediatrics, Microbial Pathogenesis, and Public Health at Yale School of Medicine, jointly published a paper detailing how this approach can be applied to treating hookworm infestations. Previous research had suggested that hookworms manipulate the human immune system by mimicking a key human regulator with their own protein, AceMIF. Together, Lolis and Cappello’s research teams screened a chemical library of almost a thousand FDA-approved compounds for possible drugs that could inhibit AceMIF activity, effectively preventing a hookworm from shutting down the human’s immune response. From this study, they were able to identify two potential anti-hookworm drugs previously tested for other purposes: sodium meclofenamate, an anti-inflammatory drug, and furosemide, a diuretic. Recently, the National Institute of Health, through their National Center for Advancing Translational Sciences (NCATS), launched a massive $20 million program to reopen research into 58 drugs shelved by various pharmaceutical companies. Worth up to $2 million each, these grants will be awarded to proposals from academics, non-profit groups, and biotechnology corporations investigating novel applications for these failed drugs. Even this effort, however, has not been without controversy. Some, like former Pfizer President John LaMattina, have criticized the NCATS undertaking, claiming that companies themselves have already taken similar rediscovery initiatives. Others worry about potential intellectual property issues that may impede the process to push the repurposed drug through to the clinic. Companies may be hesitant to sacrifice any measure of intellectual property rights of their compounds, which are central to their value. On the other hand, without patent protection, researchers will have a difficult time convincing companies to continue developing off-patent drugs and bring them to market. Although advances in both biological understanding and computational technology offer exciting possibilities in old drugs, the road to the clinic remains long and treacherous.
The Food and Drug Administration (FDA) Thursday approved the first retinal implant for use in the United States. The FDA’s green light for Second Sight’s Argus II Retinal Prosthesis System gives hope to those blinded by a rare genetic eye condition called advanced retinitis pigmentosa, which damages the light-sensitive cells that line the retina. For Second Sight, FDA approval follows more than 20 years of development, two clinical trials and more than $200 million in funding—half from the National Eye Institute, the Department of Energy and the National Science Foundation, and the rest from private investors. The Argus II has been approved for use in Europe since 2011 and implanted in 30 clinical-trial patients since 2007. The FDA’s Ophthalmic Devices Advisory Panel in September 2012 voted unanimously to recommend approval. The Argus II includes a small video camera, a transmitter mounted on a pair of eyeglasses, a video processing unit and a 60-electrode implanted retinal prosthesis that replaces the function of degenerated cells in the retina, the membrane lining the inside of the eye. Although it does not fully restore vision, this setup can improve a patient’s ability to perceive images and movement, using the video processing unit to transform images from the video camera into electronic data that is wirelessly transmitted to the retinal prosthesis. Retinitis pigmentosa—which affects about one in 4,000 people in the US and about 1.5 million people worldwide—kills the retina’s photoreceptors, the rod and cone cells that convert light into electrical signals transmitted via the optic nerve to the brain’s visual cortex for processing. Second Sight plans to adapt its technology to someday assist people afflicted with age-related macular degeneration, a similar but more common disease.
Two Indiana University researchers have developed a computer model they say can identify significantly better and less-expensive treatments than can doctors acting alone. It’s just the latest evidence that big data will have a profound impact on our health care system. How much better? They claim a better than 50 percent reduction in costs and more than 40 percent better patient outcomes. The idea behind the research, carried out by Casey Bennett and Kris Hauser, is simple and gets to the core of why so many people care so much about data in the first place: If doctors can consider what’s actually happening and likely to happen instead of relying on intuition, they should be able to make better decisions. In order to prove out their hypothesis, the researchers worked with “clinical data, demographics and other information on over 6,700 patients who had major clinical depression diagnoses, of which about 65 to 70 percent had co-occurring chronic physical disorders like diabetes, hypertension and cardiovascular disease.” They built a model using Markov decision processes — which predict the probabilities of future events based on those immediately preceding them — and dynamic decision networks — which extend the Markov processes by considering the specific features of those events in order to determine the probabilities. Essentially, their model considers the specifics of a patient’s current state and then determines the best action to effect the best possible outcome. Specifically, Bennett and Hauser found via a simulation of 500 random cases that their model decreased the cost per unit of outcome change to $189 from the $497 without it, an improvement of 58.5 percent. They found their original model improved patient outcomes by nearly 35 percent, but that tweaking a few parameters could bring that number to 41.9 percent. IBM has been banging this drum loudly, most recently with two new commercial versions of its Watson system — one of which is designed to determine the best-possible course of treatment for lung cancer patient by analyzing their situations against a library of millions of pages of clinical evidence and medical research. So, although we won’t hear “Paging Dr. Watson” at the hospital anytime soon, there’s an increasingly high chance our doctors will retire to their offices with our charts and ask a computer system of some sort what might be wrong with us and how they might best fix it.
After years of research, the first bionic eye has seen the light of day in the United States, giving hope to the blind around the world. Developed by Second Sight Medical Products, the Argus II Retinal Prosthesis System has helped more than 60 people recover partial sight, with some experiencing better results than others. Consisting of 60 electrodes implanted in the retina and glasses fitted with a special mini camera, Argus II has already won the approval of European regulators. The US Food and Drug Administration is soon expected to follow suit, making this bionic eye the world's first to become widely available. "It's the first bionic eye to go on the market in the world, the first in Europe and the first one in the U.S.," said Brian Mech, the California-based company's vice president of business development. Those to benefit from Argus II are people with retinitis pigmentosa, a rare genetic disease, affecting about 100,000 people in the U.S., that results in the degeneration of the retinal photoreceptors. The photoreceptor cells convert light into electrochemical impulses that are transmitted to the brain via the optic nerve, where they are decoded into images. "The way the prosthesis works (is) it replaces the function of the photoreceptors," Mech told AFP. Thirty people aged 28 to 77 took part in the clinical trial for the product, all of whom were completely blind. Mech said the outcomes varied by participant. "We had some patients who got just a little bit of benefit and others who could do amazing things like reading newspaper headlines," he said.
A new 3D printing process using human stem cells could pave the way to custom replacement organs for patients, eliminating the need for organ donation and immune suppression, and solving the problem of transplant rejection. The process, developed at Edinburgh-based Heriot-Watt University, in partnership with Roslin Cellab, could also speed up and improve the process of reliable, animal-free drug testing by growing three-dimensional human tissues and structures for pharmaceuticals to be tested on.
Via Ray and Terry's
Technique could be sensitive enough to detect structure of a single protein. Diamond-based quantum devices can now make nuclear magnetic resonance measurements on the molecular scale. Work by two independent groups will make it easier to find out the structure of single biological molecules such as proteins without destroying or freezing them. Nuclear magnetic resonance (NMR) and its close cousin magnetic resonance imaging (MRI) give information about a sample’s structure by detecting the weak magnetic forces in certain atomic nuclei, such as hydrogen. They work by detecting how molecules collectively resonate — like guitar strings that vibrate together — with electromagnetic waves of specific wavelengths. The techniques provide information about the structure of samples without damaging them — which is particularly important if the sample is a human body. But to some researchers, whole bodies are less interesting than the molecules that they are made up of. “I want to push NMR and MRI to the molecular level,” says Friedemann Reinhard, a physicist at the University of Stuttgart in Germany. His team is one of two that have used NMR to detect hydrogen atoms in samples measuring just a few nanometers across. Probing single molecules a few nanometres wide has been a major frustration in NMR. The detectors need to be a similar size to the sample, and the magnetic coils usually used cannot easily be made smaller than a few micrometers.
NMR and MRI measurements on the nanoscale have been done using powerful nanomagnets in a technique called magnetic resonance force microscopy — but that only worked with very cold samples. Rugar and Reinhard took a different approach. Both teams made diamonds with defects in their crystal structure — a single nitrogen atom next to a missing carbon atom, a few nanometres below the surface. This gives the diamond a red fluorescent glow, which can be bright or dull depending on which way the nitrogen’s electrons are spinning.
Dual-hormone artificial pancreas is a step closer for patients with type 1 diabetes. Randomized trial shows improved glucose levels, lower risk of hypoglycemia.
It is challenging for patients with type 1 diabetes to control their glucose levels because tight glucose control increases the incidence of hypoglycemia (dangerously low glucose levels). Insulin pump treatment, which provides a continuous predetermined subcutaneous supply of insulin, is available, but hypoglycemia still occurs. "Hypoglycemia is feared by most patients and remains the most common adverse effect of insulin therapy," writes Ahmad Haidar, Institut de Recherches Cliniques de Montréal and McGill University, with coauthors. The dual-hormone artificial pancreas delivers insulin and glucagon using infusion pumps based on continuous glucose sensor readings as guided by an intelligent dosing algorithm. The infusion pumps and the glucose sensors are already on the market, but the intelligent algorithm was developed by the researchers in Montreal.
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Analyzing queries made to Google, Bing, and other search engines can reveal the potentially dangerous consequences of mixing prescriptions before they are known to the Food and Drug Administration (FDA), according to a new study. Such data mining could even expose medical risks that slip through clinical trials undetected. Pharmaceuticals often have side effects that go unnoticed until they're already available to the public. This is especially true of side effects that emerge when two drugs interact, largely because drug trials try to pinpoint the effects of one drug at a time. Physicians have a few ways to hunt for these hidden risks, such as reports to FDA from doctors, nurses, and patients. One study, in 2011, data-mined those FDA reports and uncovered a hidden drug interaction: When taken together, the antidepressant paroxetine and the cholesterol suppressant pravastatin cause hyperglycemia, or high blood sugar. After verifying that finding with experiments, the researchers behind the study wondered what other information sources were left untapped. Enter search engines. Much like Google Flu Trends reveals influenza outbreaks by tracking flu-related search terms, search queries about drug combinations and possible side effects—say, "paroxetine," "pravastatin," and "hyperglycemia"—might enable researchers to identify unanticipated downsides to medications, says bioinformatics researcher Nigam Shah of Stanford University in Palo Alto, California. "If a lot of people are concerned about a symptom, that in itself is valuable information." Although many bad reactions to drugs never get reported to doctors, people talk about what's bothering them all the time on a casual basis to their friends or online, notes computational biologist Nicholas Tatonetti of Columbia University, who was also involved with the study. "They don't really know," he says. "They're just reporting on their symptoms, which is just a normal thing that humans love to do." Before anyone knew about the drug combination's side effects, one out of 10 people searching for both drugs also looked for terms related to hyperglycemia—about twice as often as did people looking up paroxetine or pravastatin alone. The researchers then looked for 62 other drug pairings, half known to cause hyperglycemia and the other half known not to. They found that the data-mining procedure correctly predicted whether the drug combo did or did not cause hyperglycemia about 81% of the time. The findings add yet another resource for scientists to find clues to drug risks, Shah says, and this one can be monitored in real time. One hope, he notes, is that search engine companies could analyze the data and ship the results to FDA, which would then screen the information and alert doctors of new potential risks. "This is information, we have access to it. As a society we're sitting on it," he says. "We could use it to assist the FDA, which currently relies on the reported sources." The new study is "exciting" because the field is so new, says biomedical informatics researcher Hojjat Salmasian of Columbia University, who was not involved with the work. "We don't know how much potential it has," he says. "But based on the results that have been published so far in this study and other similar studies, it seems like this is a very important field to explore."
Temporary electronic tattoos could soon help people fly drones with only thought and talk seemingly telepathically without speech over smartphones, researchers say. Commanding machines using the brain is no longer the stuff of science fiction. In recent years, brain implants have enabled people to control robotics using only their minds, raising the prospect that one day patients could overcome disabilities using bionic limbs or mechanical exoskeletons. But brain implants are invasive technologies, probably of use only to people in medical need of them. Instead, electrical engineer Todd Coleman at the University of California at San Diego is devising noninvasive means of controlling machines via the mind, techniques virtually everyone might be able to use. His team is developing wireless flexible electronics one can apply on the forehead just like temporary tattoos to read brain activity. “We want something we can use in the coffee shop to have fun,” Coleman says. The devices are less than 100 microns thick, the average diameter of a human hair. They consist of circuitry embedded in a layer or rubbery polyester that allow them to stretch, bend and wrinkle. They are barely visible when placed on skin, making them easy to conceal from others. The devices can detect electrical signals linked with brain waves, and incorporate solar cells for power and antennas that allow them to communicate wirelessly or receive energy. Other elements can be added as well, like thermal sensors to monitor skin temperature and light detectors to analyze blood oxygen levels. Using the electronic tattoos, Coleman and his colleagues have found they can detect brain signals reflective of mental states, such as recognition of familiar images. One application they are now pursuing is monitoring premature babies to detect the onset of seizures that can lead to epilepsy or brain development problems. The devices are now being commercialized for use as consumer, digital health, medical device, and industrial and defense products by startup MC10 in Cambridge, Mass.
In recent years, a plethora of bionic hands have emerged for amputees. However, surveys of those using such artificial hands have revealed that up to 50 percent of amputees do not use theprosthesis regularly, due to poor functionality, appearance and controllability. So, to improve the amount of dexterity and sensation of these bionic hands, scientists reasoned they could use interfaces that link the hands with the nervous system, potentially enabling intuitive control and realistic sensory feedback. "Our dream is to have Luke Skywalker getting back his hand with normal function," researcher Silvestro Micera told TechNewsDaily, referencing the hero in "Star Wars" who gets an artificial hand after his real one is cut off. Micera is the head of the translational neural engineering lab at the Swiss Federal Institute of Technology in Lausanne, Switzerland, which is one of the collaborators helping to develop the new bionic hand.
In a four-week clinical trial, Micera and his colleagues found they could improve the sensory feedback an amputee received from bionics by using electrodes implanted into the median and ulnar nerves in the arm near the stump. This helped deliver feelings of touch. In addition, the researchers analyzed motor neural activity from the nerves, signals used to help control muscles. They found they could tease out signals related to grasping to help control a prosthetic hand placed near the amputee but not physically attached to the person's arm. In other words, it may be possible to develop an artificial hand that can transmit signals to and respond to data from the brain. "We could be on the cusp of providing new and more effective clinical solutions to amputees in the next years," Micera said.
Take a walk through a human brain? Fly over the surface of Mars? Computer scientists at the University of Illinois at Chicago are pushing science fiction closer to reality with a wraparound virtual world where a researcher wearing 3-D glasses can do all that and more. In the system, known as CAVE2, an 8-foot-high screen encircles the viewer 320 degrees. A panorama of images springs from 72 stereoscopic liquid crystal display panels, conveying a dizzying sense of being able to touch what's not really there. As far back as 1950, sci-fi author Ray Bradbury imagined a children's nursery that could make bedtime stories disturbingly real. "Star Trek" fans might remember the holodeck as the virtual playground where the fictional Enterprise crew relaxed in fantasy worlds. The Illinois computer scientists have more serious matters in mind when they hand visitors 3-D glasses and a controller called a "wand." Scientists in many fields today share a common challenge: How to truly understand overwhelming amounts of data. Jason Leigh, co-inventor of the CAVE2 virtual reality system, believes this technology answers that challenge. "In the next five years, we anticipate using the CAVE to look at really large-scale data to help scientists make sense of that information. CAVEs are essentially fantastic lenses for bringing data into focus," Leigh said. The CAVE2 virtual world could change the way doctors are trained and improve patient care, Leigh said. Pharmaceutical researchers could use it to model the way new drugs bind to proteins in the human body. Car designers could virtually "drive" their vehicle designs. Imagine turning massive amounts of data – the forces behind a hurricane, for example – into a simulation that a weather researcher could enlarge and explore from the inside. Architects could walk through their skyscrapers before they are built. Surgeons could rehearse a procedure using data from an individual patient. But the size and expense of room-based virtual reality systems may prove insurmountable barriers to widespread use, said Henry Fuchs, a computer science professor at the University of North Carolina at Chapel Hill, who is familiar with the CAVE technology but wasn't involved in its development. While he calls the CAVE2 "a national treasure," Fuchs predicts a smaller technology such as Google's Internet-connected eyeglasses will do more to revolutionize medicine than the CAVE. Still, he says large displays are the best way today for people to interact and collaborate.
Cornell bioengineers and physicians have created an artificial ear - using 3-D printing and injectable molds - that looks and acts like a natural ear, giving new hope to thousands of children born with a congenital deformity called microtia. Over a three-month period, these flexible ears grew cartilage to replace the collagen that was used to mold them. "This is such a win-win for both medicine and basic science, demonstrating what we can achieve when we work together," said co-lead author Lawrence Bonassar, associate professor of biomedical engineering. The novel ear may be the solution reconstructive surgeons have long wished for to help children born with ear deformity, said co-lead author Dr. Jason Spector, director of the Laboratory for Bioregenerative Medicine and Surgery and associate professor of plastic surgery at Weill Cornell. "A bioengineered ear replacement like this would also help individuals who have lost part or all of their external ear in an accident or from cancer," Spector said. Replacement ears are usually constructed with materials that have a Styrofoam-like consistency, or sometimes, surgeons build ears from a patient's harvested rib. This option is challenging and painful for children, and the ears rarely look completely natural or perform well, Spector said. To make the ears, Bonassar and colleagues started with a digitized 3-D image of a human subject's ear and converted the image into a digitized "solid" ear using a 3-D printer to assemble a mold. They injected the mold with collagen derived from rat tails, and then added 250 million cartilage cells from the ears of cows. This Cornell-developed, high-density gel is similar to the consistency of Jell-O when the mold is removed. The collagen served as a scaffold upon which cartilage could grow. The process is also fast, Bonassar added: "It takes half a day to design the mold, a day or so to print it, 30 minutes to inject the gel, and we can remove the ear 15 minutes later. We trim the ear and then let it culture for several days in nourishing cell culture media before it is implanted." The incidence of microtia, which is when the external ear is not fully developed, varies from almost 1 to more than 4 per 10,000 births each year. Many children born with microtia have an intact inner ear, but experience hearing loss due to the missing external structure.
As you read this sentence, on average at least one person in the US will have started to clutch her chest. The blood flow to her heart will become blocked and cardiac muscle cells will start to die off and get replaced with scar tissue. This person has just suffered a heart attack and most likely will go on to develop heart failure, a weakening of the heart’s ability to pump blood and oxygen. In five years time, there’s a 50/50 chance she’ll be dead. There are currently no treatments that can repair the damage associated with this so-called ‘myocardial infarction’ (MI), but a potential solution is now showing promise in a large-animal model. A team of bioengineers at the University of California–San Diego (UCSD) has now developed a protein-rich gel that appears to help repair cardiac muscle in a pig model of MI. The researchers delivered the hydrogel via a catheter directly into the damaged regions of the porcine heart, and showed that the product promoted cellular regeneration and improved cardiac function after a heart attack. Compared to placebo-treated animals, the pigs that received a hydrogel injection displayed a 30% increase in heart volume, a 20% improvement in heart wall movement and a 10% reduction in the amount of scar tissue scar three months out from their heart attacks. “We hope this will be a game-changing technology that can actually prevent heart failure after heart attack,” says UCSD’s Karen Christman, who led the study. Christman and her team developed their hydrogel by stripping muscle cells from pig hearts, leaving behind a network of proteins that naturally self-assembles into a porous and fibrous scaffold upon injection into heart tissue. They previously tested its safety and efficacy in rats, where they found increased cardiac function and no toxicity or cross-species reactivity. Similar strategies using naturally-derived scaffolding, such as small intestinal submucosa from pigs inwound patching, are well established. The UCSD study now shows the clinical potential of this approach for cardiac regeneration after a heart attack in a large animal that more approximates humans. Christman has already formed a company based on the technology, called Ventrix, and she hopes to move the product into human safety trials within the year.
This might be a new way to get a shot. Funded in part by the NIH, this vaccine patch [1] is coated in a thin film that literally melts into the skin when the patch is applied. The film contains DNA, rather than protein, which is absorbed by the skin cells and triggers an immune reaction. It seems to be effective in animal models. DNA vaccines are attractive because they may not require refrigeration like typical protein vaccines and can be stably stored for weeks. And, though this patch looks spiky, the length of the needles can be adjusted so that they don’t reach the skin layers that contain nerves. Thus: no pain at all. [1] Polymer multilayer tattooing for enhanced DNA vaccination. Demuth PC, Min Y, Huang B, Kramer JA, Miller AD, Barouch DH, Hammond PT, Irvine DJ. Nat Mater. 2013 Jan 27.
The adhesive strategies of marine mussels are key to their survival on wet, wind-swept, and wave-swept surfaces. Given this, mussel tenacity has become a poster child for the wet adhesion needed elsewhere in human technology, particularly in health-care delivery. Mussel adhesion is complex with both chemical and physical underpinnings at multiple length scales. The peculiar catechol-based chemistry of mussel adhesion has inspired a variety of applications ranging from hard and soft tissue repair to drug delivery to magnetic imaging agents. Although the emphasis on new bioinspired materials is inevitable, it should be coupled with the recognition that society is equally well served by the mussel byssus (holdfast) as an indicator of mussel well-being. Byssally interconnected mussel clusters are the basis of mariculture and diverse reef-like intertidal ecologies that resist coastal erosion. Given its exquisite sensitivity to environmental conditions, mussel byssus also serves as an important monitor of pollution and climate change.
To see if the compound worked in live animals, a veterinary surgeon collaborating with Messersmith's team made a 2.5-centimeter incision in the carotid artery of a dog and placed four stitches along the length of that incision to hold it in place. With the stitches alone, the incision bled when the surgeon pressed it. But just 20 seconds after the mussel-based glue was applied, the artery was sealed and didn’t bleed. More recently, Messersmith’s team began testing its glue on fetal membranes. For the past few decades, surgeons have begun surgically repairing birth defects like spina bifida while a fetus is still in utero. But the process is risky because the surgery risks rupturing the fetal membrane prematurely, sending the mother into premature labor. This can lead to the birth of a tiny, vulnerable preemie. There are no good adhesives on the market for surgeons to repair such fetal-membrane tears, and that’s the major reason fetal surgery remains risky. But in recent, unpublished experiments in rabbits, Messersmith and colleagues found that after a veterinary surgeon poked a 3.5-mm hole in the animal’s fetal membrane, the new, mussel-inspired glue readily sealed up the puncture. What’s more, without the glue, only 40% of the fetal rabbits survived the surgery, but with the glue, 60% did. In another recent result that’s in press at Advanced Health Materials, the researchers chemically altered the polyethylene glycol polymer so that the glue would shrink when it hardened. This could counter tissue swelling during surgery, which surgeons say is dangerous. And the fetal surgeons working with Messersmith are testing whether the glue can help reseal the tissue surrounding the spinal cord to repair a serious birth defect known spinal bifida in rabbits. “It seems like exactly what you want to seal up an artery,” says Emily Carrington, a biologist at the University of Washington’s Friday Harbor Laboratories who studies mussel adhesion and who did not take part in the research. The mussel-inspired glue is ideal, she added, because it is both strong and it has give. “I think it’s very exciting.”
A medical device company with a needlefree glucose monitoring system that keeps a constant read of glucose levels in the blood has achieved positive clinical trial results in a study to monitor patients in a critical care setting. The study at Tufts University included 15 adult patients scheduled for elective cardiac surgery. Echo Therapeutics’ (NASDAQ: ECTE) device, the Symphony tCGM biosensor, was applied to the patients’ skin site prior to surgery. Blood samples were collected from the arterial line catheters every 30 minutes and measured with a glucose analyzer. The 540 Symphony tCGM glucose readings for the study subjects were paired with reference blood glucose measurements and showed that more than 99 percent of the readings were clinically accurate with no benign errors. The needle-free, transdermal device is designed to be more efficient and less invasive for patients in hospital settings. Although critical care patients have been in its initial target, the company sees plenty of scope for the device to be used in the daily ritual of diabetics checking their levels. Although there are several glucose monitoring systems on the market or being developed, Dr. Patrick Mooney’s Echo’s CEO and chairman said its device has a better error rate than its rivals and can give continuous readings. Mooney also sees potential for the device for transdermal drug delivery, a market valued at $5.6 billion.
Help may be on the way for people with compromised immune systems, severe allergies, or who otherwise have to be wary of airborne nasties. A team of scientists have created something known as a soft x-ray electrostatic precipitator, or an SXC ESP for short. It filters all manner of bacteria, allergens, viruses, and ultrafine particles from the air – plus, it kills everything it catches.
Via Ray and Terry's
Pluripotent stem cells have the ability to become any cell in the human body including, skin, blood and brain matter. Once the stem cells have begun to differentiate, the challenge for researchers is to control the process and produce only the desired, specific cells.
Using a technology known as fluorescence activated cell sorting (FACS), Associate Professor Barberi and his team were able to identify the precise combination of protein markers expressed in the lens epithelium that enabled them to isolate those cells from the rest of the cultures. Most markers are common to more than one type of cell, making it challenging to determine the exact mix of markers unique to the desired cells.
Associate Professor Barberi said this breakthrough would eventually help cure visual impairment caused by congenital cataracts or severe damage to the lens from injury through lens transplants.
"The lens has, to some extent, the ability to heal well following surgical intervention. However, with congenital cataracts, the fault is wired into the DNA, so the lens will re-grow with the original impairment. This problem is particularly prevalent in developing countries," he said.
Combined with advances in producing pluripotent stem cells from fully-differentiated adult cells, the research will also progress treatments for eye diseases.
"In the future, we will be able to take adult skin cells, for example, and turn back the clock to produce stem cells. From there, using processes like we have developed for lens epithelium, we will be able to produce diseased cells - an invaluable asset for medical research," Associate Professor Barberi said.
To get a clear picture of what’s happening inside a cell, scientists need to know the locations of thousands of proteins and other molecules. MIT chemists have now developed a technique that can tag all of the proteins in a particular region of a cell, allowing them to more accurately map those proteins.
“That’s a holy grail for biology — to be able to get spatially and temporally resolved molecular maps of living cells,” says Alice Ting, the Ellen Swallow Richards Associate Professor of Chemistry at MIT. “We’re still really far from that goal, but the overarching motivation is to get closer to that goal.”
Ting’s new method, developed with researchers from the Broad Institute and Harvard Medical School, combines the strengths of two existing techniques — microscopic imaging and mass spectrometry — to tag proteins in a specific cell location and generate a comprehensive list of all the proteins in that area.
In a paper appearing in the Jan. 31 online edition of Science, Ting and colleagues used the new technique to identify nearly 500 proteins located in the mitochondrial matrix — the innermost compartment of the cellular organelle where energy is generated.
Using fluorescence or electron microscopy, scientists can determine protein locations with high resolution, but only a handful of a cell’s approximately 20,000 proteins can be imaged at once. “It’s a bandwidth problem,” Ting says. “You certainly couldn’t image all the proteins in the proteome at once in a single cell, because there’s no way to spectrally separate that many channels of information.”
With mass spectrometry, which uses ionization to detect the mass and chemical structure of a compound, scientists can analyze a cell’s entire complement of proteins in a single experiment. However, the process requires dissolving the cell membrane to release a cell’s contents, which jumbles all of the proteins together. By purifying the mixture and extracting specific organelles, it is then possible to figure out which proteins were in those organelles, but the process is messy and often unreliable.
The new MIT approach tags proteins within living cells before mass spectrometry is done, allowing spatial information to be captured before the cell is broken apart. This information is then reconstructed during analysis by noting which proteins carry the location tag.
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