Ideally, we’re all supposed to see our doctor once a year for a checkup. It’s an opportunity to see how we’re doing from a health perspective, address any concerns or issues that we may have and catch any emerging issues before they become true problems.
But those visits are really only one-time, infrequent snapshots of health. They don’t give a full view of how we’re doing or feeling.
Now, think for a moment about how often you post something to Facebook or Twitter. Do you post anything about whether you’re feeling ill or down, or haven’t slept well? Ever share how far you ran, the route you biked or your number of steps for the day?
Every time you do, you’re creating a data point—another snapshot—about your health. Put those data points together, and what starts to emerge is a rich view of your health, much richer than one based on the records of your occasional medical visit.
Painful, tissue-damaging vaso-occlusive crises (a.k.a. pain crises) are one of the key clinical concerns in sickle cell disease (SCD). The characteristic C-shaped red blood cells of SCD become jammed in capillaries, starving tissues of oxygen and triggering searing pain. Over a patient’s life, these repeated rounds of oxygen deprivation (ischemia) can take a heavy toll on multiple organs.
There’s some debate as to why these crises take place—is the sickled cell’s shape and rigidity at fault, or are the blood vessels chronically inflamed and more prone to blockage? Either way, doctors can currently do little to treat vaso-occlusive crises, and nothing to prevent them.
Why don’t these wounds close? Blame a perfect storm of diabetic complications, such as reduced blood flow, neuropathy and impaired signaling between cells. According to research by Denisa Wagner, PhD, of Boston Children’s Hospital’s Program in Cellular and Molecular Medicine, a poorly understood feature of our immune system’s neutrophils may be one more ingredient in the storm.
Self-discovery is a theme that unites Sun Hur’s life and work. Growing up with a passion for physics, Hur pursued a scientific career in chemistry before launching her own research group in biology. Today, Hur, an investigator in Boston Children’s Hospital’s Program in Cellular and Molecular Medicine (PCMM), uses her considerable intellectual gifts to uncover how the immune system distinguishes self from non-self.
In the video above, produced by the Vilcek Foundation (which honors and supports foreign-born scientists and artists who have made outstanding contributions to society in the United States), Hur talks about her personal and scientific journey since coming to the U.S. from her native South Korea in 2000. Overcoming cultural and language barriers, she has turned her childhood fascination with order and chaos toward exploring how the innate immune system recognizes invaders, in particular disease-causing viruses that generate a double-stranded RNA during replication.
Responding to Chinese scientists’ attempt to use CRISPR gene editing technology to edit human embryos, the White House spoke up, saying, “altering the human germline for clinical purposes is a line that should not be crossed at this time.”
Your child’s forehead is warm, and you just took her temperature. The next question is, what to do about it? We all know that an average normal temp is 98.6°F, but is 100° a problem? Should 102° be a concern?
This is where Thermia comes in. It’s an online fever calculator developed by the HealthMap team at Boston Children’s Hospital. Essentially, it’s an educational tool aimed at helping concerned parents interpret a child’s temperature and understand which steps they should consider taking.
“I’m a father of two, and I still wonder sometimes what a temperature actually means,” says HealthMap co-founder John Brownstein, PhD. “We realized that there really aren’t any fever calculators out there to help parents answer that question.
“Our idea with Thermia,” he adds, “was to arm families with information so they don’t panic when their child has a temperature.”
[Update 5/18/15: According to a Wyss Institute press release, the Design Museum in London has selected the organs-on-chips as the winner of their 2015 Designs of the Year exhibition’s Product category.]
If you’re in New York City in the next few months, pop into the Museum of Modern Art (MoMA) and stop by the “This Is For Everyone: Design For The Common Good” exhibit. There—alongside displays dedicated to the “@” symbol, the pin icon from Google Maps and bricks made from living mushroom roots—you’ll find three small silicone blocks mounted on a wall panel.
Earlier this month, MoMA announced its plans to include the chips as part of their exploration of contemporary design in the digital age. In the museum’s eyes, organs-on-chips are more than a way to model disease in a complex, living system—they’re also art.
One of the immune system’s basic jobs is to tell “self” from “non-self.” Our cells carry markers that the immune system uses to recognize them as being part of us. Cells that don’t carry those markers—like bacteria and other pathogens—therefore don’t belong.
Cancer cells, however, fall into a gray area. They’re non-self, yet they also bear markers that connote self-ness—one of the reasons the immune system has a hard time “seeing” and reacting to cancer.
Can we focus the immune system’s spotlight on cancer cells? The provisional answer is yes. Research on cancer immunotherapy—treatments that spur an immune response against cancer cells—has boomed in recent years. (The journal Science recognized cancer immunotherapy as its Breakthrough of the Year in 2013.)
Allergies of all kinds—to food, pollen, pets, etc.—can be blamed on a kind of antibody called IgE. Cousins of the more common IgG, IgE antibodies work with immune cells called mast cells to trigger the symptoms we associate with an allergic reaction (itchy skin, runny nose, closing throat, etc.).
Edda Fiebiger, PhD, has been studying IgE and allergies for years, and has noticed a curious association in several epidemiologic studies: people with high levels of IgE in their blood (as in people with allergies) have a lower risk of certain cancers. This—and the discovery of human IgE antibodies that bind to tumor antigens—suggests that IgE may help protect the body from cancer, and has given rise to a whole new field dubbed AllergoOncology.
But how does it work? In a recent paper in Cell Reports, Fiebiger and her colleagues reveal a pathway by which IgE may keep watch for tumor cells, one that’s totally separate from its allergic role.