Author: Tom Ulrich

So, what’s your digital phenotype?

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.

As John Brownstein, PhD—director of the Computational Epidemiology Group (CEG) in Boston Children’s Hospital’s Computational Health Informatics Program and the hospital’s new Chief Innovation Officer—explains in this episode of the Harvard Medical School (HMS) Labcast (click the image above to hear it), this view has a name: your digital phenotype.

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Targeting inflammation in sickle cell disease with fatty acids

sickle cell disease red blood cells
(OpenStax College/Wikimedia Commons)

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.

The inflammation view, however, is leading some researchers to ask whether omega-3 fatty acids—which can alleviate inflammation—might be part of the solution. A recent mouse study in the journal Haematologica, led by Mark Puder, MD, PhD, of Boston Children’s Vascular Biology Program, and Carlo Brugnara, MD, of the hospital’s Department of Laboratory Medicine reveals some molecular clues and suggests that human trials of omega-3s might be a good next step.

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How our neutrophils might sabotage wound healing in diabetes

When you get a cut or a scrape, your body jumps into action, mobilizing a complicated array of cells and factors to stem bleeding, keep the wound bacteria-free and launch the healing process.

For most of us, that process is complete in a couple of weeks. But for many people with type 1 and type 2 diabetes, delayed wound healing can have permanent consequences. For example, between 15 and 25 percent of diabetes patients develop chronic foot ulcers. Those ulcers are the root cause of roughly two-thirds of lower limb amputations related to diabetes.

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.

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Sun Hur, PhD: Overcoming barriers to reveal innate immunity’s secrets

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.

These studies, which could open doors to new treatments for cancer and inflammatory diseases, recently garnered her the Vilcek’s 2015 Prize for Creative Promise in Biomedical Science.

Adapted from announcements originally published by the Vilcek Foundation and the PCMM.

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What we’ve been reading: Week of May 25, 2015

paszczak000/Flickr https://www.flickr.com/photos/paszczak000/3311707373/
(paszczak000/Flickr)

The White House draws the line against CRISPR/Cas9-designed embryos (FierceBiotechResearch)

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.”

Smartphones put medical diagnostics in your hands (Chemical & Engineering News)

Could smartphones help monitor disease outbreaks? Screen patients for cancer? Diagnose HIV? With the right attachments and data, the answer could one day be yes.

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Clinicians and social media: Finding the right relationship

doctor_social_media_shutterstock_264246836_260x260I remember the day about 15 years ago when my doctor tentatively gave me his email address, telling me he trusted that I wouldn’t abuse it. (For the record, I’ve used that address maybe five times.)

Fast forward to today, where doctors and nurses are frequently on social media the same as the rest of us, usually behaving well, sometimes not.

What place do social media have in a physician or nurse’s career? And where do the boundaries lie?

Read the full story on Boston Children’s Hospital’s new blog for healthcare providers, Notes.

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Is that fever a problem? Ask Thermia

Thermia fever calculator HealthMap

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.”

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The design world’s eyes are on organs-on-chips

Organs-on-chips Museum of Modern Art MoMA London Design Museum exhibit Wyss Institute Vascular Biology
Organs-on-chips on display in New York City’s Museum of Modern Art. (Photo: Wyss Institute at Harvard University)

[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.

Those blocks are actually three of the organs-on-chips developed in the lab of Donald Ingber, MD, PhD, founding director of the Wyss Institute for Biologically Inspired Engineering and a scientist in Boston Children’s Hospital’s Vascular Biology Program.

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.

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Targeting leukemia with a clinical trial of CAR T-cell therapy

relapsed leukemia targeted therapy CAR T-cell immunotherapy

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.)

And one of the more recent methods—called chimeric antigen receptor (CAR) T-cell therapy—is now in a clinical trial for relapsed or treatment-resistant B-cell acute lymphoblastic leukemia (ALL) at the Dana-Farber/Boston Children’s Cancer and Blood Disorders Center.

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Looking beyond allergies: Does IgE keep a wary eye out for cancer?

watchdog IgE allergies cancer

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.

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