Boston Children’s Hospital’s science stories are getting a new home. To keep up with the latest research at Boston Children’s Hospital, you can now visit our new all-hospital hub, Discoveries, and click the “Research” tab.
The new site will also keep you up to date on clinical news,
patient stories, parenting tips, our favorite photos and videos and community
We hope you’ll bookmark Discoveries and check in often. In the meantime, the Vector blog will remain online as an archive for research stories from April 2019 and earlier.
Eczema, a chronic itchy inflammatory skin disease, affects
about 15 percent of U.S. children. It’s a strong risk factor for food allergies
— more than half of children with eczema are allergic to one or more foods — and
most people with food allergy have eczema. But the connection between the two
hasn’t been clear. New
research in a mouse model demonstrates, for the first time, that scratching
the skin promotes allergic reactions to foods, including anaphylaxis.
Newborns with life-threatening congenital heart disease often undergo open-heart surgery with cardiopulmonary bypass, which carries a risk of damaging the brain. Critically ill newborns who are placed on ECMO are at even higher risk for brain injury. Hypothermia, or cooling the body, can improve neurologic outcomes, but has limitations.
A new study in a large animal model suggests that adding a dash of hydrogen to the usual mix of respiratory gases could further protect babies’ brains.
Surgeons have used robots operated by joysticks for more than a decade, and teams have shown that tiny robots can be steered through the body by external forces such as magnetism. Now, a paper in Science Robotics describes a robotic catheter that can navigate autonomously — the surgical equivalent of a self-driving car.
Bioengineers at Boston Children’s Hospital demonstrated a robotic catheter that found its way along the walls of a beating, blood-filled heart to a leaky valve in an animal model, without a surgeon’s involvement.
the heart is fully formed, the cells that make up heart muscle, known as cardiomyocytes,
have very limited ability to reproduce themselves. After a heart attack, cardiomyocytes
die off; unable to make new ones, the heart instead forms scar tissue. Over
time, this can set people up for heart failure.
New work published last week in Nature Communications advances the possibility of reviving the heart’s regenerative capacities using microRNAs — small molecules that regulate gene function and are abundant in developing hearts.
In 2013, Da-Zhi Wang, PhD, a cardiology researcher at Boston Children’s Hospital and a professor of pediatrics of Harvard Medical School, identified a family of microRNAs called miR-17-92 that regulates proliferation of cardiomyocytes. In new work, his team shows two family members, miR-19a and miR-19b, to be particularly potent and potentially good candidates for treating heart attack.
Three children Alejandro Gutierrez, MD, treated for leukemia during his fellowship at Boston Children’s Hospital still haunt him more than a decade later. One 15-year-old boy died from the toxicity of the drugs he was given; the other two patients went through the whole treatment only to die when their leukemia came back. “That really prompted a deep frustration with the status quo,” Gutierrez recalls. “It’s motivated everything I’ve done in the lab since then.”
Gutierrez, now a researcher in the Division of Hematology/Oncology, has made it his mission to figure out why leukemia treatments cure some patients but not others. And in today’s issue of Cancer Cell, he and 15 colleagues report progress on two important fronts: They shed light on how leukemia cells become resistant to drugs, and they describe how two drugs used in combination may overcome that resistance, offering new hope to thousands of children and adults with leukemia.
Does exposure to stress early in life affect a baby’s brain development, and is there a way to single out babies who might benefit from early intervention? A two-center study led by Boston Children’s Hospital, published today in JAMA Pediatrics, used brain EEGs to begin to get at these questions in an objectively measurable way. It found that infants whose mothers reported high levels of stress have a distinct pattern of brain activity as measured by EEG — at only 2 months of age.
“The EEG has been found to be exquisitely sensitive to perturbations in the environment, and thus we are not entirely surprised to see an association between stress in a mother’s life and her infant’s brain activity,” says Charles Nelson, PhD, director of the Laboratories of Cognitive Neuroscience at Boston Children’s Hospital and the study’s senior investigator. “What we were surprised by, in part, was how early in life we see this association.”
In 1989, two undergraduate students at the Free University
of Brussels were asked to test frozen blood serum from camels, and stumbled on
a previously unknown kind of antibody. It was a miniaturized version of a human
antibody, made up only of two heavy protein chains, rather than two light and
two heavy chains. As they
eventually reported, the antibodies’ presence was confirmed not only in
camels, but also in llamas and alpacas.
Fast forward 30 years. In the journal PNAS this week, researchers at Boston Children’s Hospital and MIT show that these mini-antibodies, shrunk further to create so-called nanobodies, may help solve a problem in the cancer field: making CAR T-cell therapies work in solid tumors.
The ability to edit genes in patients’ blood
stem cells — which produce red blood cells, platelets, immune cells and more — offers
the potential to cure many genetic blood disorders. If all goes well, the
corrected cells engraft in the bone marrow and produce healthy, properly
functioning blood cells… forever.
But scientists have had difficulty introducing
edits into blood stem cells. The efficiency and specificity of the edits and
their stability once the cells engraft in the bone marrow have been variable.
A new approach, described this week in Nature Medicine and in January in the journal Blood, overcomes prior technical challenges, improving the efficiency, targeting and durability of the edits. Researchers at Dana-Farber/Boston Children’s Cancer and Blood Disorders Center and the University of Massachusetts Medical School successfully applied the technique to two common blood diseases — sickle cell disease and beta thalassemia — involving mutations in the gene for beta globin protein.
The human immune system includes about a dozen major cell
types with specialized roles in the body’s defenses. They serve as sentries,
identify threats, mobilize troops, capture and transport invaders, interrogate
and kill those deemed dangerous and clear the battlefield of casualties. This intricate
command-and-control system is what enables us to fend off most of the dangerous
bacteria and viruses that come our way.
But in patients who suffer from inflammatory bowel disease (IBD), the immune system itself becomes the enemy. Even when the body faces no threat, immune cells called “helper T cells” take up arms, resulting in a kind of perpetual warfare that — far from being helpful — causes collateral damage to the gut.
“The system goes into overdrive,” says Yu Hui Kang, an
immunology graduate student at Harvard Medical School and a researcher at
Boston Children’s Hospital.
“These cells have gone too far, and they can’t stop.”
Now Kang and colleagues in the lab of Scott Snapper, MD, PhD, director of Boston Children’s Inflammatory Bowel Disease Center, may have found a way to turn the tables on the immune system by recruiting its own “natural killer” cells to wipe out the harmful T cells. Though clinical applications are years away, the work suggests new avenues for developing treatments for the debilitating disease.