Deprivations common in orphanages, from lack of social contact to endless routines, can lower children's IQs. But foster homes can help them bounce back, according to the first controlled study on the topic, led by Charles Nelson, PhD, research director of Children's Developmental Medicine Center. Preschoolers abandoned to Romanian institutions had lower IQs than children in biological families. But children taken into quality foster homes nearly caught up, particularly if placed before age 2. (Science, Dec. 21, 2007)
Premature babies face the world too early, with underdeveloped lungs. Those born at 7 months or earlier risk a second assault: inflammation in which the body "chews up" the lungs, leading to lifelong lung disease. Now, gene-chip studies of these babies' umbilical cords, led by Isaac Kohane, MD, PhD, director of the Children's Hospital Informatics Program, suggest a way to predict the inflammation within hours of birth—and even a way to prevent it. The researchers found that a certain biochemical pathway is disrupted only in babies who progress to inflammation and lung disease. Interestingly, the same pathway is disrupted in adult chronic obstructive pulmonary disease. Drugs targeting that pathway are already in development for adults, and might offer hope for premature infants. (Genome Biology, Oct. 2007)
Melanoma, a deadly cancer that resists chemotherapy, now looks a lot more vulnerable. In 2005, Children's scientists discovered a protein on melanoma cells that acts like a bouncer, ejecting toxic substances like chemotherapy drugs. Now, Markus Frank, MD, of the joint Children's’Ä́Brigham and Women's Hospital Transplantation Research Center, has found that this protein, called ABCB5, is unique to the deadliest cells in melanoma—the stem cells that keep it growing. Using antibodies, they leveraged this protective protein, luring the body to attack the cells that bear it. When mice received the treatment, growth of implanted human melanoma tumors was strongly inhibited. (Nature, Jan. 17, 2008)
Dyslexia can be hard to diagnose, treat or even define, because of its various origins. But two Children's researchers are finding clues in the brain that give insight into the condition. Studying patients with a rare genetic disorder, Chris Walsh, MD, PhD, chief of Genetics at Children's, traced a form of dyslexia marked by poor reading fluency (slow, choppy reading) to disorganized tracts of nerve fibers in the brain. Nadine Gaab, PhD, of Children's Laboratory of Cognitive Neuroscience, found that training the ear to distinguish sounds can improve reading—and even rewire the brain—in dyslexic children whose problems stem from faulty auditory processing. She's now looking for ways to detect and correct sound-processing problems before children even start school. (Restorative Neurology and Neuroscience, Oct. 16, 2007; Neurology, Dec. 4, 2007.)
While many genes are linked to muscular dystrophy and related disorders of muscle weakness and wasting, it's poorly understood how these genes cause disease, and, more importantly, how to translate that knowledge into treatments. Louis Kunkel, PhD, director of Children's Program in Genomics, looked at microRNAs, bits of code that govern genes, and found that some are out of balance in wasting muscle—either too abundant or too scarce. These microRNAs could lead the researchers to as-yet undiscovered genes involved in muscle degeneration, Kunkel says, and might themselves make more efficient targets for therapy than individual genes. (PNAS, Oct. 2007)
Scientists have long wondered why patients with the skin condition eczema often develop asthma. Now, a mouse study by Raif Geha, MD, chief of Immunology at Children's, makes it clear. When patients with eczema scratch, immune cells in their blood contact allergens on their skin. The immune system readies a defense, and if patients later inhale more allergens, the immune system wages a full-scale attack in the lungs. Stringing together this response is a messenger called interleukin-17. Geha hopes that blocking this messenger will stop asthma in patients with eczema. (PNAS, Oct. 2007)
About 1 percent of people worldwide with autism spectrum disorders have a piece of chromosome 16 that either duplicates or goes missing, a new study finds. Adding to the roughly 15 percent of cases with known genetic causes, the abnormality most often happens during embryonic development and isn't usually inherited. A Children's team led by Bai-Lin Wu, PhD, director of the Genetics Diagnostic Laboratory, found it using the latest microarray technology, confirming and extending parallel studies by the Boston-wide Autism Consortium. The missing/duplicated piece contains some 25 genes whose function can now be explored further. In the meantime, Children's has a diagnostic test available for families. (New England Journal of Medicine, Jan. 9, 2008)
Zebrafish are genetically similar to humans, so make good models for studying human disease. Now, Richard White, MD, PhD, in Children's Stem Cell Program, has bred a zebrafish that is transparent throughout its life, allowing researchers to directly view its internal organs and observe disease processes like tumor growth or engraftment of bone marrow transplants in a living organism. White created the transparent fish—called Casper—by breeding zebrafish without stripes with zebrafish lacking reflective pigment. Viewing Casper under a low-power microscope, White saw, for the first time, single cancer cells proliferating and metastasizing from a tumor. (Cell Stem Cell, Feb. 7, 2008)