Can your smart watch detect when you are becoming sick? A new study from Stanford, publishing January 12th, 2017 in PLOS Biology, indicates that this is possible.
By following 60 people through their everyday lives, Stanford researchers found that smart watches and other personal biosensor devices can help flag when people have colds and even signal the onset of complex conditions like Lyme disease and diabetes. “We want to tell when people are healthy and also catch illnesses at their earliest stages,” said Michael Snyder, PhD, Professor and Chair of Genetics at Stanford and senior author of the study. Postdoctoral scholars Xiao Li, PhD, and Jessilyn Dunn, PhD, and researcher Denis Salins share lead authorship.
Smart watches and similar portable devices are commonly used for measuring steps and physiological parameters, but have not generally been used to detect illness. Snyder’s team took advantage of the portability and ease of using wearable devices to collect a myriad of measurements from participants for up to two years to detect deviations from their normal baseline for measurements such as heart rate and skin temperature. Because the devices continuously follow these measures, they potentially provide rapid means to detect the onset of diseases that change your physiology.
Many of these deviations coincided with times when people became ill. Heart rate and skin temperature tends to rise when people become ill, said Snyder. His team wrote a software program for data from a smart watch called ‘Change of Heart’ to detect these deviations and sense when people are becoming sick. The devices were able to detect common colds and in one case helped detect Lyme disease–in Snyder, who participated in the study.
“I had elevated heart rate and decreased oxygen at the start of my vacation and knew something was not quite right,” said Snyder. After running a low-grade fever for several days, Snyder visited a physician who confirmed the illness. Snyder took the antibiotic doxycycline and the symptoms disappeared. Subsequent tests confirmed the presence of Lyme. The smart watch and an oxygen sensor were useful in detecting the earliest signs of illness.
This research paves the way for the smart phone to serve as a health dashboard, monitoring health and sensing early signs of illness, likely even before the person wearing it does.
In addition to detecting illness, the study had several other interesting findings. Individuals with indications of insulin resistance and who are therefore are at high risk for Type 2 diabetes are often unaware that they have this risk factor. Personal biosensors could potentially be developed into a simple test for those at risk for Type 2 diabetes by detecting variations in heart rate patterns, which tend to differ from those not at risk.
Another interesting finding of the study is an effect that impacts many of us. The authors found that blood oxygenation decreases during airplane flights. Although this is a known effect, the authors were able to characterize it in greater detail than has been previously reported. Snyder’s team found that reduced blood oxygenation typically occurs for a large fraction of a flight and further demonstrated that this is associated with fatigue. “Many of us have had the experience of feeling tired on airplane flights,” Snyder said. “Sometimes people may attribute this to staying up late, a hectic work schedule, or the stress of travel. However, it is likely that cabin pressure and reduced oxygen also are contributors.”
“The information collected could aid your physician, although we can expect some initial challenges in how to integrate the data into clinical practice,” said Snyder. For example, patients may want to protect the privacy of their physiologic data or may want to share only some of it.
“Physicians and third-party payers will demand robust research to help guide how this comprehensive longitudinal personal data should be used in clinical care,” Snyder said. “However, in the long-term I am very optimistic that personal biosensors will help us maintain healthier lives.”
The new cells prevented the onset of diabetes in an animal model of the disease bringing personalized cell therapy for diabetes closer.
Scientists at the Gladstone Institutes and the University of California, San Francisco (UCSF) have successfully converted human skin cells into fully-functional pancreatic cells. The new cells produced insulin in response to changes in glucose levels, and, when transplanted into mice, the cells protected the animals from developing diabetes in a mouse model of the disease.
The new study, published in Nature Communications, also presents significant advancements in cellular reprogramming technology, which will allow scientists to efficiently scale up pancreatic cell production and manufacture trillions of the target cells in a step-wise, controlled manner. This accomplishment opens the door for disease modeling and drug screening and brings personalized cell therapy a step closer for patients with diabetes.
An excess of bacteria in the gut can change the way the liver processes fat and could lead to the development of metabolic syndrome, according to health researchers.
Metabolic syndrome is a group of conditions including obesity, type 2 diabetes, high blood pressure, high blood sugar and excess body fat around the waist. People experiencing three or more of these conditions are considered to have metabolic syndrome and are vulnerable to liver and heart diseases. Approximately 20 to 25 percent of adult Americans have the syndrome, according to the American Heart Association.
Research supported by the National Institutes of Health has recommended that Americans add more fiber to their diets because higher fiber diets have been found to improve many aspects of health. However in a certain segment of the population, this advice could be doing more harm than good.
Publishing in the journal Chemistry and Biology, the researchers found that activating AMPK with compound 14 led to a reduction in fasting blood glucose levels, improved glucose tolerance and, at the same time, promoted weight loss in obese mice.
When mice with a normal diet were treated with compound 14, their blood glucose levels and weight remained normal.
In obese mice on the high-fat diet a single dose of compound 14 resulted in lowering their elevated blood glucose close to near normal levels.
A daily dose of compound 14 administered for seven days to the obese mice resulted in improved glucose tolerance and 1.5 grams weight loss.
A multidisciplinary research team discovers how cells know to rush to a wound and heal it — opening the door to new treatments for diabetes, heart disease and cancer
Researchers at the University of Arizona have discovered what causes and regulates collective cell migration, one of the most universal but least understood biological processes in all living organisms.
The findings, published in the March 13, 2015, edition of Nature Communications, shed light on the mechanisms of cell migration, particularly in the wound-healing process. The results represent a major advancement for regenerative medicine, in which biomedical engineers and other researchers manipulate cells’ form and function to create new tissues, and even organs, to repair, restore or replace those damaged by injury or disease.
“The results significantly increase our understanding of how tissue regeneration is regulated and advance our ability to guide these processes,” said Pak Kin Wong, UA associate professor of mechanical and aerospace engineering and lead investigator of the research.
“In recent years, researchers have gained a better understanding of the molecular machinery of cell migration, but not what directs it to happen in the first place,” he said. “What, exactly, is orchestrating this system common to all living organisms?”
Leaders of the Pack
The answer, it turns out, involves delicate interactions between biomechanical stress, or force, which living cells exert on one another, and biochemical signaling.
The UA researchers discovered that when mechanical force disappears — for example at a wound site where cells have been destroyed, leaving empty, cell-free space — a protein molecule, known as DII4, coordinates nearby cells to migrate to a wound site and collectively cover it with new tissue. What’s more, they found, this process causes identical cells to specialize into leader and follower cells. Researchers had previously assumed leader cells formed randomly.
Wong’s team observed that when cells collectively migrate toward a wound, leader cells expressing a form of messenger RNA, or mRNA, genetic code specific to the DII4 protein emerge at the front of the pack, or migrating tip. The leader cells, in turn, send signals to follower cells, which do not express the genetic messenger. This elaborate autoregulatory system remains activated until new tissue has covered a wound.
The same migration processes for wound healing and tissue development also apply to cancer spreading, the researchers noted. The combination of mechanical force and genetic signaling stimulates cancer cells to collectively migrate and invade healthy tissue.
Biologists have known of the existence of leader cells and the DII4 protein for some years and have suspected they might be important in collective cell migration. But precisely how leader cells formed, what controlled their behavior, and their genetic makeup were all mysteries — until now.
Broad Medical Applications
“Knowing the genetic makeup of leader cells and understanding their formation and behavior gives us the ability to alter cell migration,” Wong said.
With this new knowledge, researchers can re-create, at the cellular and molecular levels, the chain of events that brings about the formation of human tissue. Bioengineers now have the information they need to direct normal cells to heal damaged tissue, or prevent cancer cells from invading healthy tissue.