Pancreatic cancer has become the third leading cause of cancer mortality. Its incidence is rising in parallel with the rise in obesity, and it’s hard to treat: five-year survival still hovers at just 8 to 9 percent. A new study published online in Nature Communications finds early success with a completely new, metabolic approach: reducing tumors’ ability to get rid of excess nitrogen.
The researchers, led by Nada Kalaany, PhD, of Boston Children’s Hospital’s Division of Endocrinology and the Broad Institute of MIT and Harvard, provide evidence that targeting the enzyme arginase 2 (ARG2) can curb pancreatic tumor growth, especially in people who are obese.
“We found that highly malignant pancreatic tumors are very dependent on the nitrogen metabolism pathway,” says Kalaany. …
Botulism is a rare, potentially fatal paralyzing illness. It’s the reason we shouldn’t feed infants honey and why we need to take care in consuming home-canned foods: they can potentially contain nerve-damaging toxins produced by Clostridium botulinum. Botulinum toxin is classified as one of the six most dangerous potential bioterrorism agents.
There are seven known types of botulinum toxin. Toxins A and B were first identified in 1919, and first purified in 1946 and 1947, respectively. (Both are also used medically.) Toxins C, D, E and F eventually followed. The last, toxin G, was identified in 1969 in soil bacteria in Argentina.
And that’s where it’s stood until now. But to truly defend against botulism, we need to know all the toxins made by the various C. botulinum strains, since each requires a separate antibody to neutralize it. …
It’s been a challenge to develop a surgical adhesive that sticks to wet surfaces and isn’t toxic. But it turns out a certain kind of slug is very good at secreting a sticky mucus that glues fast, apparently as a defense mechanism.
That provided the inspiration for a hydrogel “super” adhesive that could supplant surgical sutures, at least for some operations, and help medical devices stay in place. Researchers at the Wyss Institute for Biologically Inspired Engineering and Harvard’s School of Engineering and Applied Sciences (SEAS), led by David Mooney, PhD, report that the adhesive bound strongly to a variety of animal tissues, including skin, cartilage, artery, liver and heart.
Nikolay Vasilyev, MD, a coauthor on the paper, is interested in the adhesive’s potential for young patients with congenital heart disease. He is is a research scientist in Cardiac Surgery at Boston Children’s Hospital, and led cardiac studies in pig models. …
Two-year-old Vanessa had survived the unthinkable: two massive cerebral hemorrhages, nine days apart. Katherine Bell and her wife Nancy Mendoza felt immense relief at their daughter’s close call. But they wanted to know more. What had caused Vanessa’s strokes? Would there be more? Was the cause treatable?
A 4-year-old has a progressively enlarging head and loss of developmental milestones: a clear case of hydrocephalus. He undergoes a minimally invasive endoscopic third ventriculostomy (ETV) to drain off the trapped cerebrospinal fluid.
This requires puncturing the floor of the brain’s third ventricle (fluid-filled cavity) with an endoscope — while avoiding a lethal tear in the basilar artery, which lies perilously close.
There are no good neurosurgical training models for this rare and scary operation.
“We semi-blindly poke a hole through the ventricle floor,” says Benjamin Warf, MD, director of Neonatal and Congenital Anomaly Neurosurgery at Boston Children’s Hospital. “To make the technique safer and to be able to train more people, it would be very helpful to make that hole in a way that’s less anxiety-provoking.” …
Over the past decade, mutations to more than 60 different genes have been linked with autism spectrum disorder (ASD), including de novo mutations, which occur spontaneously and aren’t inherited. But much of autism still remains unexplained.
A new study of nearly 6,000 families implicates a hard-to-find category of de novo mutations: those that occur after conception, and therefore affect only a subset of cells. Findings were published today in Nature Neuroscience. …
When infants see or hear something interesting to them, like the sound of a human voice, their heart rate tends to slow down ever so slightly, a sign they’re paying attention. But a recent small study suggests this may not be true for infants at risk for autism.
Researchers led by Katherine Perdue, PhD, of the Laboratories of Cognitive Neuroscience at Boston Children’s Hospital, studied 40 babies who had an older sibling with autism spectrum disorder (ASD). These “baby sibs” are at 20-fold risk for developing autism themselves. For comparison, Perdue and colleagues also studied 48 infants who did not have a sibling with ASD and were therefore at low risk for autism.
At 3, 6, 9 and 12 months of age, the at-risk infants had slower heartbeats than the low-risk infants. When the babies were presented with speech sounds, heart rates slowed less in the at-risk babies than in the low-risk infants.
While none of the at-risk infants, followed until age 2, were later diagnosed with ASD, the researchers believe they may still be at risk for problems such as delayed speech. This may be due to differences in auditory processing. “It might not be autism per se, but it could be something that’s related to communication in some way,” Perdue told Spectrum News.
How did our distinctive brains evolve? What genetic changes, coupled with natural selection, gave us language? What allowed modern humans to form complex societies, pursue science, create art?
While we have some understanding of the genes that differentiate us from other primates, that knowledge cannot fully explain human brain evolution. But with a $10 million grant to some of Boston’s most highly evolved minds in genetics, genomics, neuroscience and human evolution, some answers may emerge in the coming years.
The Seattle-based Paul G. Allen Frontiers Group today announced the creation of an Allen Discovery Center for Human Brain Evolution at Boston Children’s Hospital and Harvard Medical School. It will be led by Christopher A. Walsh, MD, PhD, chief of the Division of Genetics and Genomics at Boston Children’s and a Howard Hughes Medical Institute investigator.
“To understand when and how our modern brains evolved, we need to take a multi-pronged approach that will reflect how evolution works in nature, and identifies how experience and environment affect the genes that gave rise to modern human behavior,” Walsh says. …
About 1 out of 100 babies are born with a congenital heart defects. Thanks to medical and surgical advances, these children usually survive into adulthood, but they are often left with developmental, behavioral or learning challenges.
Children with “single-ventricle” defects — in which one of the heart’s two pumping chambers is too small or weak to function properly — are especially at risk for neurodevelopmental problems. “Single-ventricle physiology creates cerebrovascular hemodynamics that can reduce oxygen delivery to the brain,” explains Jane Newburger, MD, MPH, director of the Cardiac Neurodevelopmental Program at Boston Children’s Hospital.
How does this play out in adolescence? In three recent studies, Boston Children’s Heart Center collaborated with the departments of Neurology and Psychiatry to track neurodevelopmental outcomes after corrective Fontan operations. They evaluated preteens and teens as old as 19 — the longest follow-up to date. …
Getting a damaged optic nerve to regenerate is vital to restoring vision in people blinded through nerve trauma or disease. A variety of growth-promoting factors have been shown to help the optic nerve’s retinal ganglion cells regenerate their axons, but we are still far from restoring vision. A new study published yesterday in Neuron underscores the complexity of the problem.
A research team led by Fengfeng Bei, PhD, of Brigham and Women’s Hospital, Zhigang He, PhD, and Michael Norsworthy, PhD, of Boston Children’s Hospital, and Giovanni Coppola, MD, of UCLA conducted a screen for transcription factors that regulate the early differentiation of RGCs, when axon growth is initiated. While one factor, SOX11, appeared to be critical in helping certain kinds of RGCs regenerate their axons, it simultaneously killed another type — alpha-RGCS (above)— when tested in a mouse model.
At least 30 types of retinal ganglion cell message the brain via the optic nerve. “The goal will be to regenerate as many subtypes of neurons as possible,” says Bei. “Our results here suggest that different subtypes of neurons may respond differently to the same factors.”