In 2006, Matt Walliser, now chief engineer at San Francisco-based Blossom Coffee, took on an internship at the Carnegie Mellon Innovations Laboratory at NASA Research Park, part of Ames Research Center in Moffett Field, California. He spent four summers at the lab and at Ames' Exploration Aerial Vehicles (EAV) Laboratory, starting when he was a high school student and continuing while he worked toward his mechanical engineering degree. There, he worked on a class of control systems—proportional-integral-derivative (PID) controllers—that is common on rockets, missiles and other aircraft. PID controllers work by continually monitoring and correcting the output of a controlled system through feedback loops. Among other purposes, the team in Ames' lab used the technology to keep rovers moving at constant speeds over varying terrain. But after graduation, Walliser realized the technique could also help make better coffee. Coffee made from the same beans can taste significantly different when brewed at different temperatures, Walliser explains. "Most coffee machines will control the temperature within five to 10 degrees, but the average coffee drinker can tell the difference between coffees brewed as little as two degrees apart." But how to control the temperature more accurately? Walliser figured PID controllers could help. He was working with Jeremy Kuempel, who had approached him with his idea for a high-end, precision coffee maker. The two would found Blossom Coffee Inc. in 2011. Drawing on the expertise he developed at Ames, Walliser enabled Blossom's machine, called the Blossom One Brewer, to control the average temperature of water to within one degree. It also keeps all the coffee grounds within 10 degrees of each other, regardless of their place within the brewing basket, a temperature gradient significantly narrower than in most coffeemakers, and it automatically corrects heating and fluid delivery for altitude, barometric pressure and ambient temperature. Tight temperature controls allow the user to consistently produce the same brew. They also let the machines change temperature from one cup to the next within a few seconds. Recipes for different beans can be shared and downloaded via the Internet. Walliser calls the coffeemakers "semi-automatic," noting that, while they control temperature and extraction time, the grind and the stirring time are in the hands of the barista, making the brewing process flexible. "It's still a craft product, and you still need training to use it, but it takes over the things that are difficult to control by hand," he says. The first prototype Blossom Limited machines went on sale in 2013 for $11,111. By early 2015, the company had set up production in Japan and was offering the Blossom One for about half the price of the prototype. The current product is a single-cup brewer marketed to cafés and coffee shops, but Walliser says the company hopes to offer a home version in the future. Walliser credits the freedom interns have while working in the NASA labs for the innovations he's developed. "Being able to do engineering in a self-directed manner isn't an experience you usually get in high school, or even college," he says. "Having that kind of real-world experience really allowed me to excel in school and build the skills I have today." Explore further: Used coffee grounds are a rich source of healthful antioxidants
A new passenger jet that can fly at supersonic speeds without the distinctive but earsplitting sonic "boom" generated when these superfast planes travel faster than the speed of sound is one step closer to getting in the air. NASA has awarded a contract to Lockheed Martin Aeronautics to come up with a preliminary design for the supersonic jet. The company will receive $20 million over 17 months to come up with a preliminary design, according to NASA. The Lockheed team includes individuals from GE Aviation and Tri Models Inc., acting as subcontractors, the agency said. NASA envisions a "low boom" aircraft that emits a supersonic "heartbeat," or a soft thump, rather than startlingly noisy sonic booms, when it breaks the sound barrier. At the end of its contract, Lockheed will be expected to outline the proposed jet's baseline requirements and design in order to meet NASA's expectations for the agency's Quiet Supersonic Technology (QueSST) program. [Supersonic! The 10 Fastest Military Airplanes] After a demonstration version of the jet is built, the vehicle will undergo analytical and wind-tunnel tests, according to NASA. "Developing, building and flight testing a quiet supersonic X-plane is the next logical step in our path to enabling the industry's decision to open supersonic travel for the flying public," Jaiwon Shin, associate administrator for NASA's Aeronautics Research Mission Directorate, said in a statement. Once the jet is ready for flight tests, NASA will conduct low-boom flight demonstrations to gauge the public's response to quieter supersonic planes. The actual design and construction of the QueSST jet will be awarded under a future contract, NASA officials said. The loud booms generated by supersonic aircraft prompted the U.S. Federal Aviation Administration to ban overland flights by these aircraft in 1973. NASA, however, said in a previous statement that it is working with the FAA to change those regulations. [Image Gallery: Breaking the Sound Barrier] "We are working with other agencies across the world to support development of new noise certification for supersonic flight, so instead of being prohibited, it would be allowed over land and sea," Alexandra Loubeau, an acoustics engineer at NASA's Langley Research Center in Hampton, Virginia, said in a statement released in late 2015. The QueSST jet is the first in a series of X-planes that will receive funding in NASA's fiscal 2017 budget, as a part of the agency's New Aviation Horizons initiative. The initiative aims to make future aircraft safer, "greener" and more efficient, using metrics such as fuel use, emissions and noise to judge their performance. The first flights under NASA's New Aviation Horizons initiative are expected to begin around 2020, depending on funding, the agency said. Copyright 2016 LiveScience, a Purch company. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
News Article | January 9, 2016
The Kepler spacecraft is back in action and NASA has confirmed that it has found over 100 planets orbiting stars. Ian Crossfield from the University of Arizona announced the mission's discoveries at an American Astronomical Society conference Tuesday, noting that the revamped Kepler mission, now known as K2, found some planets different from what the original mission observed. Many of these were orbit stars and multi-planet systems hotter and brighter than those from the original Kepler field. For instance, K2 spotted a system with three planets bigger than Earth, found a planet within the Hyades star cluster and discovered a planet in the process of being ripped apart while orbiting a white dwarf star. "It's probing different types of planets [than the original Kepler mission]. ... The idea here is to find the best systems, the most interesting systems," said Tom Barclay from NASA's Ames Research Center. According to Crossfield, the first five of the K2 campaigns each observed a different part of the sky and found 7,000 transit-like signals. These signals went through a validation process to narrow down the planet candidates, which were then validated. A $600-million mission, Kepler was launched in 2009 with the task of determining how Earth-like planets commonly occur in the Milky Way galaxy. Over the course of four years, the mission discovered more than 1,000 planets, a number more than half of all the exoplanets that had been discovered. The Kepler spacecraft had been looking at the same patch of sky since it was launched, but it lost the ability to stare at the same spot in 2013. It underwent a few tweaks to get it back in order, resulting in the K2, but it can no longer observe the same spot indefinitely. With K2, the same patch of sky can only be observed for about 80 days at a time. Aside from observing planets as they orbit other stars, K2 is also on the lookout for supernovas and studying planets in the solar system. The mission logged a 70-day observation of Neptune in 2014 to study the planet's windy weather and is currently staring at Uranus. Afterwards, K2 is set to observe an asteroid population sharing Jupiter's orbit. The revamped Kepler mission is also looking at trying to spot planets wandering the galaxy without their own stars.
News Article | February 6, 2016
We've been taught all our lives that one of the best ways to mitigate the effects of climate change is by planting more trees that could absorb and reduce levels of carbon dioxide in the atmosphere. Turns out, this doesn't always lead to the desired effect, a new study revealed. Switching to dark conifer trees from broad-leafed ones may have contributed to the rise of average temperatures in Europe. Researchers from France noted that changes in forest management have pushed summer temperatures in the continent to increase by 0.12 degree Celsius (0.2 degree Fahrenheit) since 1750. Many European nations had decided to plant conifer trees such as spruce and pines. These trees' dark colors trap the sun's heat and allow more sunlight to be absorbed, scientists said. Aside from that, conifers are more conservative with water. Kim Naudts, lead author of the study, said this leads to less evapotranspiration - the process in which water is transferred from land to the atmosphere by evaporation from the soil and transpiration by plants - and drier air, which had also contributed to warming. On the other hand, broad-leafed trees with light colors and flat leaves -- including birch and oak trees -- reflect more sunlight back into space. As Europe expanded its forests to conifers, however, it had to give up its broad-leafed trees. Fast-growing conifers dominated forests and everything else since then. Conifers stretched to additional 633,000 square kilometers (244,000 miles) of land, while broad-leafed cover was reduced by 436,000 square kilometers (168,000 miles). Thus, the effect took place. While increasing conifer cover should have had a positive effect on the climate, researchers found that forests in Europe accumulated a "carbon debt." This meant that European forests have released 3.1 billion metric tons of carbon into the planet's atmosphere since the switch to conifers occurred. How so? Naudts said humans had extracted wood from unmanaged forests, removing their capacity to store carbon. "Even a well-managed forest today stores less carbon than its natural counterparts in 1750," said Naudts. "If the point is to store carbon, then afforestation is presumably good, but losing carbon to wood extraction is bad," added Richard Houghton, an ecologist from the Woods Hole Research Center. But it's not all about carbon. Naudts said government policies regarding forest management should be re-considered to take into account other factors such as the color of trees and their changes to moistures and soils. Researchers concluded that European forests have not resulted to the climate benefit that some might have hoped for. "Two and a half centuries of forest management in Europe have not cooled the climate," the authors of the study wrote. It may not even be an isolated case, although the study is restricted to Europe. Experts say similar effects are likely to be occurring in other parts of the world with big forest planting programs, including the United States, Russia and China. Another study conducted by the European Commission provides evidence that could support Naudts' and her team's findings. The report, which is featured in the journal Science, found that the loss of forests all over the world has led to an increase in maximum and average global temperatures, particularly in tropical and arid regions.
In cancer research, no success is more revered than the huge reduction in deaths from childhood leukaemia. From the 1960s to the 2000s, researchers boosted the number of children who survived acute lymphoblastic leukaemia from roughly 1 in 10 to around 9 in 10. What is sometimes overlooked, however, is that these dramatic gains against the most common form of childhood cancer were made not through the invention of new drugs or technologies, but rather through a reassessment of the tools in hand: a dogged analysis of the relative gains from different medicines and careful strategizing over how best to apply them side by side as combination therapies. “It wasn't just about pounding drugs together,” says Jedd Wolchok, a medical oncologist at Memorial Sloan Kettering Cancer Center in New York City. “It was about understanding the mechanism and figuring out what should be given when.” That lesson has particular relevance in cancer research today. A new class of immunotherapies — which turn the body's immune system against cancerous cells — is elevating hopes about combination therapies again. The drugs, called checkpoint inhibitors, have already generated great excitement in medicine when applied on their own. Now there are scores of trials mixing these immune-boosting drugs with one another, with radiation, with chemotherapies, with cancer-fighting viruses, with cell treatments and more. “The field is exploding,” says Crystal Mackall, who leads the paediatric cancer immunotherapy programme at Stanford University in California. Fast-moving trends in cancer biology often fail to meet expectations, and little is yet known about how these drugs work together. Some observers warn that the combinations being tested are simply marriages of convenience — making use of readily available compounds or capitalizing on business alliances. “In many cases, we're moving forward without a rationale,” says Alfred Zippelius, an oncologist at the University of Basel in Switzerland. “I suspect we'll see some disappointment in the next few years with respect to immunotherapy.” But many clinicians argue that delay is not an option as their patients queue up for the next available clinical trial. “Right now I have more patients that could benefit from combinations than there are combinations being tested,” says Antoni Ribas, an oncologist at the University of California, Los Angeles. “We're always waiting on the next slot.” Immunotherapies have been more than a century in the making, starting when physicians first noticed mysterious remissions in a few people with cancer who contracted a bacterial infection. The observations led to a hypothesis: perhaps the immune system is able to kill tumours when made hypervigilant by an infection. The concept has vast appeal. What better way to beat a fast-evolving biological system such as a tumour than with a fast-evolving biological immune system? But it took decades for researchers to turn that observation into something useful. Part of the trouble, they eventually learned, is that tumours suppress the immune response. T cells, the immune system's weapon of choice against cancer, would sometimes gather at the edge of a tumour and then just stop. It turned out that a class of molecules called inhibitory checkpoint proteins was holding those T cells at bay. These proteins normally protect the human body from unwarranted attack and autoimmunity, but they were also limiting the immune system's ability to detect and fight tumours. In 1996, immunologist James Allison, now at the University of Texas MD Anderson Cancer Center in Houston, showed that switching off a checkpoint protein called CTLA-4 helped mice to fend off tumours1. The discovery suggested that there was a way to re-mobilize T cells and beat cancer. In 2011, the US Food and Drug Administration (FDA) approved the first checkpoint inhibitor — a drug, called ipilimumab, that inhibits CTLA-4 — to treat advanced melanoma. The improvements were modest: about 20% of patients benefited from ipilimumab, and the survival gain was less than four months on average2. But a handful of recipients are still alive a decade after starting the therapy — a stark contrast with most new cancer drugs, which often benefit more patients in the short term, but don't have a durable response (see 'Desperately seeking survival'). Ipilimumab was at the leading edge of a flood of checkpoint inhibitors to enter clinical trials. The drug's developer, Bristol-Myers Squibb of New York, followed up with the approval of nivolumab, which inhibits the protein PD-1. And a host of other companies have jumped into the immunotherapy fray, as have academics such as Edward Garon at the University of California, Los Angeles. “Our group gladly shifted into this,” says Garon, who began focusing on checkpoint inhibitors in 2012. “It was very clear this was going to have a major impact.” But even as the family of checkpoint inhibitors was rapidly expanding, the drugs were running up against the same frustrating wall: only a minority of patients experienced long-lasting remission. And some cancers — such as prostate and pancreatic — responded poorly, if at all, to the drugs. Further research revealed a possible explanation: many people who were not responding well to the drugs were starting the treatment without that phalanx of T cells waiting at the margins of their tumours. (In the lingo of the field, their tumours were not inflamed.) Researchers reasoned that if they could raise this T-cell response first, and recruit the cells to the edges of the tumour, they might get a better result with the checkpoint inhibitors. That realization fuelled a rush to test combinations of drugs (see 'Combinatorial explosion'). Radiation and some chemotherapies kill enough tumour cells to release proteins that the immune system might then recognize as foreign and attack. Vaccines containing these proteins, called antigens, could have a similar effect. “On some level, one can make an argument for almost any drug combining well with an immunotherapy,” says Garon. “And obviously we know not all of them will.” One of the first combinations to be tested was made up of two immunotherapies — ipilimumab and nivolumab — at once. Although the targets of these drugs both do the same job, silencing T cells, they do so in different ways: CTLA-4 prevents the activation of T cells; PD-1 blocks the cells once they have infiltrated the tumour and its environment. And treating mice with compounds that block both proteins yielded a more-inflamed tumour as well3. “There was reason to think that if you block both, the T cells will be even more ready to kill the tumours,” says Michael Postow, an oncologist at Memorial Sloan Kettering. Together, ipilimumab and nivolumab boost response rates in people with advanced melanoma from 19% with just ipilimumab to 58% with the combination4. The combination also produces more-dangerous side effects than using either drug alone, but physicians are learning how to treat immunotherapy reactions, says Postow. Ipilimumab generally doesn't help people with lung cancer when given on its own, but researchers are now testing it with nivolumab. Normally, they would not have bothered to investigate a combination involving a drug that had failed on its own, Garon says. The new approach is grounded in immunology, but some researchers worry that the effort could be wasted, he adds. Researchers are also testing inhibitors of other checkpoint proteins, including TIM-3 and LAG-3, in combination with those that block PD-1. The combination approach is breathing life into drugs that had been shelved. For example, a protein called CD40 stimulates immune responses and has shown promise against cancer in animals. But in the wake of disappointing early clinical trials, some companies put their CD40 drugs to the side. Years later, mouse studies showed that combining CD40 drugs with a checkpoint inhibitor could boost their effect. Now, at least seven companies are developing them. Cancer immunologists have listed the protein as one of the targets they are most interested in studying, says Mac Cheever, a cancer immunologist at the Fred Hutchinson Cancer Research Center in Seattle, Washington. Cancer vaccines — long pursued by researchers but burdened by repeated failures in clinical trials — may also see a renaissance. There are now more than two dozen trials of cancer vaccines that make use of a checkpoint inhibitor. Some promising combinations have been uncovered by serendipitous clinical observations. Researchers at Johns Hopkins University in Baltimore, Maryland, were conducting trials of epigenetic drugs, which alter the chemical tags on chromosomes. They shifted a handful of people with lung cancer who had not responded to the drugs to a clinical trial of nivolumab. Five of them responded — a much higher proportion than expected. The discovery became the seed for an ongoing clinical trial launched in 2013 to study combinations of epigenetic drugs and immunotherapies. Preclinical work has now provided evidence that epigenetic drugs can affect aspects of the immune response. These chance observations could lead to real advances, says Wolchok. “We're riding the wave of enthusiasm.” But extracting the most from these combinations will require more well-designed preclinical studies to support the human ones. Just as attention to combinations of chemotherapies fuelled advances in treating paediatric leukaemias, the current combinatorial craze will require careful planning to work out the right pairings and timing of therapies. Another class of drug, known as targeted therapies, could also receive a significant boost from immunotherapy. These drugs, which target proteins bearing specific mutations, generate a high response rate when given to patients with those mutations, but the tumours often develop resistance to the drugs and come roaring back. Coupling targeted therapies with a checkpoint inhibitor, researchers reason, could yield both high response rates and durable remissions. One of the first targeted therapies for melanoma was an inhibitor that is specific to certain mutations in BRAF proteins that can drive tumour growth. However, an early attempt to combine this drug with ipilimumab was aborted when trial participants showed signs of possible liver damage5. No one was injured, but for some it was an important reminder that combinations can yield unanticipated side effects. “It was a good lesson for us to learn,” says Wolchok. “It will not be as simple as we imagined.” Paying careful attention to sample collection during clinical trials would help researchers to catch toxicity problems early, says Jennifer Wargo, a cancer researcher at MD Anderson. “We're making mistakes by looking just at clinical endpoints,” she adds. “We need to be smarter about how we run these trials.” In one of his latest trials, Wolchok wants to combine immunotherapy with a drug that targets a cellular pathway that some cancer cells use to maintain their rapid division. Cancers with mutations in this pathway, which is regulated by the protein MEK, can be extraordinarily difficult to treat. But the pathway is also important for T-cell development, so Wolchok is working to determine the right timing for the treatment. One approach could be to use a MEK inhibitor to quiet tumours in mice and to release tumour antigens. He would then wait for the T-cell response to rejuvenate before adding the immunotherapy. “You want to make sure you're not trying to activate the immune system at the same time you're turning off that signalling,” he says. Garon is watching such trials with optimism, but he's aware that there may be a limit to how well combinations will perform. He sees a cautionary tale in a drug from an earlier era that works mainly in people with a mutation in the protein EGFR. Researchers spent a decade trying to find drugs that could turn a non-responding patient into a responder. “It is now clear that there probably is no such agent,” he says. “I'm hopeful we won't be repeating that same response, but we have to watch our data cautiously.” Researchers are so ravenous for those data that the results are being unveiled at major meetings at an earlier stage than in the past, he adds. “People are getting up and presenting response rates when the number treated is five,” Garon says. “We generally have had a higher threshold than that.” He worries that presenting such early data could prompt community physicians in the audience to start making decisions on treatments before they are appropriately studied. The excitement is also fuelling a frenzy of clinical trials that are often based on speed rather than rationale. “Right now I'm kidding myself if I say I'm picking a combination because I have a scientific reason to pick it,” says Mackall. “It's likely to just be what was available.” The strategy may still produce some wins. “There is plenty of opportunity for serendipity now,” says Robert Vonderheide, who studies CD40 at the University of Pennsylvania in Philadelphia. But as the field matures, he says, this could give way to a more-systematic approach, similar to the careful planning and testing of variables used for paediatric leukaemias. Despite his concerns, Garon is excited to be a part of the immunotherapy wave. Last autumn, he and his colleagues held a banquet for the patients who had been enrolled in his first immunotherapy trials three years earlier. These were the lucky survivors — the few who had shown a dramatic response. As he looked around the table at the guests of honour, he marvelled at their recovery. All had been diagnosed with advanced lung cancer, and many had been too weak to work. Now they were talking about their families, re-embarking on careers and taking up old hobbies such as golf and running. “We've never been able to hold a banquet like that before,” he says. “I would love to hold many more.”