Smartwatches can now track your finger in mid-air using sonar

Smartwatches can now track your finger in mid-air using sonar

As mobile and wearable devices such as smartwatches grow smaller, it gets tougher for people to interact with screens the size of a matchbook.

That could change with a new sonar technology developed by University of Washington computer scientists and electrical engineers that allows you to interact with mobile devices by writing or gesturing on any nearby surface -- a tabletop, a sheet of paper or even in mid-air.

FingerIO tracks fine-grained finger movements by turning a smartphone or smartwatch into an active sonar system using the device's own microphones and speakers.

Because sound waves travel through fabric and do not require a line of sight, users can even interact with a phone inside a front pocket or a smartwatch hidden under a sweater sleeve.

In a paper to be presented in May at the Association for Computing Machinery's CHI 2016 conference in San Jose, California, the UW team demonstrates that FingerIO can accurately track two-dimensional finger movements to within 8mm, which is sufficiently accurate to interact with today's mobile devices. The work was recognized with an honorable mention award by the conference.

"You can't type very easily onto a smartwatch display, so we wanted to transform a desk or any area around a device into an input surface," said lead author Rajalakshmi Nandakumar, a UW doctoral student in computer science and engineering. "I don't need to instrument my fingers with any other sensors -- I just use my finger to write something on a desk or any other surface and the device can track it with high resolution."

Using FingerIO, one could use the flick of a finger to turn up the volume, press a button, or scroll through menus on a smartphone without touching it, or even write a search command or text in the air rather than typing on a tiny screen.

FingerIO turns a smartwatch or smartphone into a sonar system using the device's own speaker to emit an inaudible sound wave. That signal bounces off the finger, and those "echoes" are recorded by the device's microphones and used to calculate the finger's location in space.

Using sound waves to track finger motion offers several advantages over cameras -- which don't work without line-of-sight when the device is hidden by fabric or another obstructions -- and other technologies like radar that require both custom sensor hardware and greater computing power, said senior author and UW assistant professor of computer science and engineering Shyam Gollakota.

"Acoustic signals are great -- because sound waves travel much slower than the radio waves used in radar, you don't need as much processing bandwidth so everything is simpler," said Gollakota, who directs the UW's Networks and Mobile Systems Lab. "And from a cost perspective, almost every device has a speaker and microphones so you can achieve this without any special hardware."

But sonar echoes are weak and typically not accurate enough to track finger motion at a high resolution. Errors of a few centimeters make it impossible to differentiate between writing individual letters or subtle hand gestures.

The UW researchers employed a type of signal typically used in wireless communication -- called Orthogonal Frequency Division Multiplexing -- and demonstrated that it can be used to achieve high-resolution finger tracking using sound. Their algorithms leverage the properties of OFDM signals to track phase changes in the echoes and correct for any errors in the finger location to achieve sub-centimeter finger tracking.

To test their approach, the researchers created a FingerIO prototype app for Android devices and downloaded it to an off-the-shelf Samsung Galaxy S4 smartphone and a smartwatch customized with two microphones, which are needed to track finger motion in two dimensions. Today's smartwatches typically only have one, which can be used to track a finger in one dimension.

The researchers asked testers to draw shapes such as stars, squiggles or figure 8s on a touchpad next to a smartphone or smartwatch running FingerIO. Then they compared the touchpad tracings to the shapes created by FingerIO's tracking.

The average difference between the drawings and the FingerIO tracings was 0.8 centimeters for the smartphone and 1.2 centimeters for the smartwatch.

"Given that your finger is already a centimeter thick, that's sufficient to accurately interact with the devices," said co-author and electrical engineering graduate student Vikram Iyer.

Next steps for the research team include demonstrating how FingerIO can be used to track multiple fingers moving at the same time, and extending its tracking abilities into three dimensions by adding additional microphones to the devices.

High-throughput screen identifies potential henipavirus drug target

The closely related Hendra and Nipah viruses (referred to jointly as henipaviruses) are deadly cousins of the more common mumps, measles, and respiratory syncytial viruses, all members of the paramyxovirus family. Henipavirus outbreaks are on the rise, but little is known about them, partly because research has to be conducted under extreme level containment conditions.

A study published on March 24, 2016 in PLOS Pathogens reports the first high-throughput RNA interference screen for host genes that are essential for live henipavirus infection of human cells, and identifies a specific cell protein called fibrillarin as a potential target for drugs against henipaviruses and other paramyxoviruses.

Henipaviruses infection is common in bats, and outbreaks in Australia and Malaysia have been linked to human contact with local fruit bats. No human vaccines or treatments exist, and because of high mortality rates (between 35 and 90% of patients known to be infected died in recent outbreaks) the viruses have been classified as biosafety-level 4 (BSL-4) pathogens the highest biosafety containment level. A multi-disciplinary research team led by Cameron Stewart of the CSIRO Australian Animal Health Laboratory in East Geelong, Victoria, systematically interfered with the function of genes in human cells to identify host genes that are needed for henipavirus infection.

In their initial screen, the researchers identified several hundred human genes whose function was necessary for successful henipavirus infection. They subsequently honed in on one of them, called fibrillarin, which codes for a protein present in the nucleolus. The nucleolus is the largest structure in the nucleus of mammalian cells and functions as the assembly room for so-called ribosomes which are subsequently exported out of the nucleus into the cytoplasm and become the protein factories of the cell.

To explore possible mechanisms, the researchers examined closely which step of the viral life cycle was blocked by interfering with fibrillarin function. Fibrillarin, they found, is not necessary for viral entry into the host cells but required for the early synthesis of viral RNA. More specifically, the researchers report that mutating the catalytic activity of fibrillarin inhibits henipavirus infection, suggesting that this human enzyme could be targeted therapeutically to combat henipavirus infections.

When they tested whether fibrillarin function was required for successful infection of human cells by other paramyxoviruses, the researchers found that this was indeed the case for all the family members tested, including the mumps and measles pathogens. This raises the potential that drugs that interfere with fibrillarin function might have broader use against all of these viruses.

To their knowledge, the researchers say, the study is the first of its kind to be conducted in a BSL-4 facility. They suggest that it "serves as a blueprint for how high-throughput RNAi screens can be performed under high biocontainment conditions."

They conclude that the study "reveals a previously unappreciated role for nucleolar proteins with methyltransferase activity such as fibrillarin in henipavirus infection, and suggests that methyltransferase enzymes represent a potential target for development of an anti-henipavirus drug."

Heart attack patients getting younger, more obese

Heart attack patients getting younger, more obese

Despite increased understanding of heart disease risk factors and the need for preventive lifestyle changes, patients suffering the most severe type of heart attack have become younger, more obese and more likely to have preventable risk factors such as smoking, high blood pressure, diabetes and chronic obstructive pulmonary disease, according to a study scheduled for presentation at the American College of Cardiology's 65th Annual Scientific Session.

The new study analyzed heart disease risk factors among more than 3,900 patients who were treated for ST-elevation myocardial infarction, or STEMI--the most severe and deadly type of heart attack--at Cleveland Clinic between 1995 and 2014.

"On the whole, the medical community has done an outstanding job of improving treatments for heart disease, but this study shows that we have to do better on the prevention side," said Samir Kapadia, M.D., professor of medicine and section head for interventional cardiology at Cleveland Clinic and the study's primary investigator. "When people come for routine checkups, it is critical to stress the importance of reducing risk factors through weight reduction, eating a healthy diet and being physically active."

A STEMI heart attack results when one of the heart's main arteries becomes completely blocked by plaque, stopping the flow of blood. Immediate medical attention can increase the chances of survival, but STEMI carries a high risk of death and disability.

Many factors are known to increase a person's heart attack risk. While some, such as age and family history, are beyond the individual's control, many risk factors can be reduced through lifestyle choices, such as exercising more, quitting smoking and adopting a heart-healthy diet.

The researchers divided the records of Cleveland Clinic's STEMI patients from 1995 to 2014 into four quartiles, each representing a span of five years. Analyzing the baseline risk factors and health conditions of patients in each grouping, they found the average age of STEMI patients decreased from 64 to 60, and the prevalence of obesity increased from 31 to 40 percent between the first five-year span and the last five-year span. The proportion of patients with diabetes increased from 24 to 31 percent, the proportion with high blood pressure grew from 55 to 77 percent, and the proportion with chronic obstructive pulmonary disease rose from 5 to 12 percent over the same period. All changes were statistically significant.

One of the most striking findings, according to study authors, was the change in smoking rates, which increased from 28 to 46 percent--a finding counter to national trends, which reflect an overall decline in smoking rates over the past 20 years. All of the other risk factor trends seen in the Cleveland Clinic study were in line with national trends.

The study also revealed a significant increase in the proportion of patients who have three or more major risk factors, which grew from 65 to 85 percent. Kapadia said the findings carry strong messages for both the medical community and the general public.

"Prevention must be kept in the forefront of primary care," Kapadia said. "Cardiac health is not just dependent on the cardiologist. The primary care physicians and the patient need to take ownership of this problem."

For patients, taking ownership means adopting a heart-healthy lifestyle early. "Don't wait until you have a diagnosed heart problem to start taking care of yourself and paying attention to your lifestyle and dietary choices. You should be working hard to avoid developing heart disease in the first place," Kapadia said.

One caveat to the study is that because helicopter transports brought a greater number of patients to Cleveland Clinic from surrounding rural areas during the course of the study period, it is possible that the observed trends reflect changes in the hospital's patient population. Study authors said this factor is likely to have had only a minor effect, if any.

Prolonged daily sitting linked to 3.8 percent of all-cause deaths

Sedentary behavior, particularly sitting, has recently become a prevalent public health topic and target for intervention. As work and leisure activities shift from standing to sitting, increased sitting time is starting taking a toll on our bodies. A new study in theAmerican Journal of Preventive Medicine found that sitting for more than three hours per day is responsible for 3.8% of all-cause mortality deaths. Investigators also estimate that reducing sitting time to less than three hours per day would increase life expectancy by an average of 0.2 years.

In order to properly assess the damaging effects of sitting, the study analyzed behavioral surveys from 54 countries around the world and matched them with statistics on population size, actuarial table, and overall deaths. Researchers found that sitting time significantly impacted all-cause mortality, accounting for approximately 433,000, or 3.8%, of all deaths across the 54 nations in the study. They also found that sitting had higher impact on mortality rates in the Western Pacific region, followed by European, Eastern Mediterranean, American, and Southeast Asian countries, respectively.

This type of information is crucial to evaluating the effect sitting has on our lives, especially in light of recent research that shows prolonged sitting is associated with an increased risk of death, regardless of activity level. Researchers now believe that periods of moderate or vigorous physical activity might not be enough to undo the detrimental effects of extended sitting.

While researchers found that sitting contributed to all-cause mortality, they also estimated the impact from reduced sitting time independent of moderate to vigorous physical activity. "It was observed that even modest reductions, such as a 10% reduction in the mean sitting time or a 30-minute absolute decrease of sitting time per day, could have an instant impact in all-cause mortality in the 54 evaluated countries, whereas bolder changes (for instance, 50% decrease or 2 hours fewer) would represent at least three times fewer deaths versus the 10% or 30-minute reduction scenarios," explained lead investigator Leandro Rezende, MSc, Department of Preventive Medicine, University of Sao Paulo School of Medicine.

Studies are beginning to show us exactly how detrimental prolonged sitting is for our health, even when coupled with exercise; however, changing habits is a difficult proposition. "Although sitting is an intrinsic part of human nature, excessive sitting is very common in modern societies," commented Rezende. "Sedentary behavior is determined by individual, social, and environmental factors, all strongly influenced by the current economic system, including a greater number of labor-saving devices for commuting, at home and work, and urban environment inequalities that force people to travel longer distances and live in areas that lack support for active lifestyles."

The results of this analysis show that reducing sitting time, even by a small amount, can lead to longer lives, but lessening time spent in chairs may also prompt people to be more physically active in general. "Although sitting time represents a smaller impact compared with other risk factors, reducing sitting time might be an important aspect for active lifestyle promotion, especially among people with lower physical activity levels," emphasized Rezende. "In other words, reducing sitting time would help people increase their volumes of physical activity along the continuum to higher physical activity levels."

The public health burden of prolonged sitting is real. Accounting for 3.8% of all-cause mortality in this study, sitting is shortening the lives of people across the world. "The present findings support the importance of promoting active lifestyles (more physical activity and less sitting) as an important aspect for premature mortality prevention worldwide, and therefore the need for global action to reduce this risk factor."

New findings in humans provide encouraging foundation for upcoming AIDS vaccine clinical trial

Some people infected with HIV naturally produce antibodies that effectively neutralize many strains of the rapidly mutating virus, and scientists are working to develop a vaccine capable of inducing such "broadly neutralizing" antibodies that can prevent HIV infection.

An emerging vaccine strategy involves immunizing people with a series of different engineered HIV proteins as immunogens to teach the immune system to produce broadly neutralizing antibodies against HIV. This strategy depends on the ability of the first immunogen to bind and activate special cells, known as broadly neutralizing antibody precursor B cells, which have the potential to develop into broadly neutralizing antibody-producing B cells.

A research team has now found that the right precursor ("germline") cells for one kind of HIV broadly neutralizing antibody are present in most people, and has described the design of an HIV vaccine germline-targeting immunogen capable of binding those B cells. The findings by scientists from The Scripps Research Institute (TSRI), the International AIDS Vaccine Initiative (IAVI) and the La Jolla Institute for Allergy and Immunology were published in Science on March 25.

"We found that almost everybody has these broadly neutralizing antibody precursors, and that a precisely engineered protein can bind to these cells that have potential to develop into HIV broadly neutralizing antibody-producing cells, even in the presence of competition from other immune cells," said the study's lead author, William Schief, TSRI professor and director, Vaccine Design of the IAVI Neutralizing Antibody Center at TSRI, in whose lab the engineered HIV vaccine protein was developed.

The body's immune system contains a large pool of different precursor B cells so it can respond to a wide variety of pathogens. But that also means that precursor B cells able to recognize a specific feature on a virus surface are exceedingly rare within the total pool of B cells.

"The challenge for vaccine developers is to determine if an immunogen can present a particular viral surface in a way that distinct B cells can be activated, proliferate and be useful," said study co-author Shane Crotty, professor at the La Jolla Institute. "Using a new technique, we were able to show -- well in advance of clinical trials -- that most humans actually have the right B cells that will bind to this vaccine candidate. It is remarkable that protein design can be so specific as to 'find' one in a million cells, demonstrating the feasibility of this new vaccine strategy."

The work offers encouraging insights for a planned Phase 1 clinical trial to test a nanoparticle version of the engineered HIV vaccine protein, the "eOD-GT8 60mer." "The goal of the clinical study will be to test safety and the ability of this engineered protein to elicit the desired immune response in humans that would look like the start of broadly neutralizing antibody development," Schief said. "Data from this new study was also important for designing the clinical trial, including the size and the methods of analysis."

In June, scientists from TSRI, IAVI and The Rockefeller University reported that the eOD-GT8 60mer produced antibody responses in mice that showed some of the traits necessary to recognize and inhibit HIV. If the eOD-GT8 60mer performs similarly in humans, additional boost immunogens are thought to be needed to ultimately induce broadly neutralizing antibodies that can block HIV.

The new work also provides a method for researchers to assess whether other new vaccine proteins can bind their intended precursor B cells. This method is a valuable tool in the design of more targeted and effective vaccines against AIDS, providing the ability to vet germline-targeting immunogens before testing them in large, time-consuming and costly clinical trials.

Looking at blood donated by healthy volunteers, the scientists found B cells that were capable of creating "VRC01-class" antibodies that recognized a critical surface patch, or epitope, of HIV. VRC01-class broadly neutralizing antibodies are a group of antibodies isolated from different individuals that appear to have developed in a very similar way, and it has been hypothesized that the starting VRC01-class B cells were very similar in the different people. The eOD-GT8 60mer is designed to engage these precursor B cells to initiate HIV broadly neutralizing antibody development.

Simple solutions for overweight kids to lose weight as the weather warms up

Simple solutions for overweight kids to lose weight as the weather warms up

Obesity is almost at epidemic proportions; it has more than doubled in children and tripled in adolescents in the past 30 years nationwide. Rosa Cataldo, DO, MPH, Director of the Healthy Weight & Wellness Center at Stony Brook Children's Hospital, says that the most effective approach to addressing weight loss in children are lifestyle-based modifications that involve parents.

"Childhood obesity is a serious -- and growing -- problem in the United States, so parents should be concerned about their child's weight," says Dr. Cataldo, "We are not talking about a few extra pounds, but rather a condition that can have a negative effect on a child's overall health."

At Stony Brook's Healthy Weight & Wellness Center, it starts with a medical assessment and monitoring. At the heart of the program are nutrition and activity level changes. Specialists work to educate the family on meal planning, label reading, food choices and recipe modifications. Fit Kids for Life, a proactive program run by Peter Morelli, MD, Pediatric Cardiologist and Medical Director, also works to improve patients' overall fitness level and calorie burning activity.

As winter transitions into spring, Dr. Cataldo stresses that now is a great time to make changes for your entire family. These are her top four tips for parents and children getting healthy together:

1. Go Outside: Being outside is an easy way to make exercise feel effortless. Bike riding, playing soccer and fooling around on a playground are just a couple of ways to play as a family. Dr. Morelli adds that kids should wear a pedometer to track their physical activity and help make sure they take at least 10,000 steps a day.

2. Stay Hydrated: Be mindful to drink water throughout the entire day, especially after exercising. Stay away from giving children sugary beverages, including juices, sodas and sports drinks.

3. Choose Fresh: This is the easiest time of the year to eat fresh foods. Head to a local farmer's market where fruits and veggies are in season and cheaper. Embrace seasonal salads and grilling on the barbecue. After fresh vegetables, frozen is the second best option.

4. Read Labels: Label reading is important year around, but checking ingredients is often a forgotten step. Make sure to pay attention to the order of the ingredients; if sugar is one of the first three listed, it's too high in sugar. Rethink the product if there's a long, laundry list of ingredients, especially with long, complicated names.

The bottom line is that obese children grow into obese adults, who can develop a long list of life-threatening illnesses or conditions that impair quality of life. However, parents can break the pattern. With early involvement, parents can set the example to help their children get and remain healthy through adulthood.

Portion control: Cells found in mouse brain that signal 'stop eating'

Portion control: Cells found in mouse brain that signal 'stop eating'

While researching the brain's learning and memory system, scientists at Johns Hopkins say they stumbled upon a new type of nerve cell that seems to control feeding behaviors in mice. The finding, they report, adds significant detail to the way brains tell animals when to stop eating and, if confirmed in humans, could lead to new tools for fighting obesity. Details of the study will be published by the journalScience on March 18, 2016.

"When the type of brain cell we discovered fires and sends off signals, our laboratory mice stop eating soon after," says Richard Huganir, Ph.D., director of the Department of Neuroscience at the Johns Hopkins University School of Medicine. "The signals seem to tell the mice they've had enough."

Huganir says his team's discovery grew out of studies of the proteins that strengthen and weaken the intersections, or synapses, between brain cells. These are an important target of research because synapse strength, particularly among cells in the hippocampus and cortex of the brain, is important in learning and memory.

In a search for details about synapse strength, Huganir and graduate student Olof Lagerlöf, M.D., focused on the enzyme OGT -- a biological catalyst involved in many bodily functions, including insulin use and sugar chemistry. The enzyme's job is to add a molecule called N-acetylglucosamine (GlcNAc), a derivative of glucose, to proteins, a phenomenon first discovered in 1984 by Gerald Hart, Ph.D., director of the Johns Hopkins University School of Medicine's Department of Biological Chemistry and co-leader of the current study. By adding GlcNAc molecules, OGT alters the proteins' behavior.

To learn about OGT's role in the brain, Lagerlöf deleted the gene that codes for it from the primary nerve cells of the hippocampus and cortex in adult mice. Even before he looked directly at the impact of the deletion in the rodents' brains, Lagerlöf reports, he noticed that the mice doubled in weight in just three weeks. It turned out that fat buildup, not muscle mass, was responsible.

When the team monitored the feeding patterns of the mice, they found that those missing OGT ate the same number of meals -- on average, 18 a day -- as their normal littermates but tarried over the food longer and ate more calories at each meal. When their food intake was restricted to that of a normal lab diet, they no longer gained extra weight, suggesting that the absence of OGT interfered with the animals' ability to sense when they were full.

"These mice don't understand that they've had enough food, so they keep eating," says Lagerlöf.

Because the hippocampus and cortex are not known to directly regulate feeding behaviors in rodents or other mammals, the researchers looked for changes elsewhere in the brain, particularly in the hypothalamus, which is known to control body temperature, feeding, sleep and metabolism. There, they found OGT missing from a small subset of nerve cells within a cluster of neurons called the paraventricular nucleus.

Lagerlöf says these cells already were known to send and receive multiple signals related to appetite and food intake. When he looked for changes in the levels of those factors that might be traced to the absence of OGT, he found that most of them were not affected, and the activity of the appetite signals that many other research groups have focused on didn't seem to be causing the weight gain, he adds.

Next, the team examined the chemical and biological activity of the OGT-negative cells. By measuring the background electrical activity in nonfiring brain cells, the researchers estimated the number of incoming synapses on the cells and found that they were three times as few, compared to normal cells.

"That result suggests that, in these cells, OGT helps maintain synapses," says Huganir. "The number of synapses on these cells was so low that they probably aren't receiving enough input to fire. In turn, that suggests that these cells are responsible for sending the message to stop eating."

To verify this idea, the researchers genetically manipulated the cells in the paraventricular nucleus so that they would add blue light-sensitive proteins to their membranes. When they stimulated the cells with a beam of blue light, the cells fired and sent signals to other parts of the brain, and the mice decreased the amount they ate in a day by about 25 percent.

Finally, because glucose is needed to produce GlcNAc, they thought that glucose levels, which increase after meals, might affect the activity of OGT. Indeed, they found that if they added glucose to nerve cells in petri dishes, the level of proteins with the GlcNAc addition increased in proportion to the amount of glucose in the dishes. And when they looked at cells in the paraventricular nucleus of mice that hadn't eaten in a while, they saw low levels of GlcNAc-decorated proteins.

"There are still many things about this system that we don't know," says Lagerlöf, "but we think that glucose works with OGT in these cells to control 'portion size' for the mice. We believe we have found a new receiver of information that directly affects brain activity and feeding behavior, and if our findings bear out in other animals, including people, they may advance the search for drugs or other means of controlling appetites."