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Recent breakthroughs and findings in faculty research.

A Myth Debunked
One of the bedrock assumptions in the world of anthropology for three decades has been the observation that the 19th-century physical anthropologist Samuel Morton doctored his field findings in comparing the brain size of white and black men in order to advance his racist theory that white men had higher IQs because their brains were bigger. The influential Harvard paleontologist Stephen Jay Gould, who wrote the seminal work The Mismeasure of Man, claimed that Morton purposely measured more than 1,000 skulls inaccurately in order to advance his racist theories.

But, according to evolutionary anthropologist Jason Lewis, an assistant instructor in the Department of Anthropology in the School of Arts and Sciences, Morton was indeed right: humans living in colder climates (Europeans) had larger brains than those living in warmer climes (Africans) because they were physically bigger. Moreover, Lewis’s research—which he began more than 10 years ago as an undergraduate at the University of Pennsylvania measuring those same skulls himself—revealed that there was no evidence that Morton, who lived around the time of the Civil War, was racist; indeed, he supported emancipation. The bum rap comes from the late Gould himself, who mistakenly made the assumption that Morton, living in a time of racial upheaval in the nation, surely was racist.

Lewis’s findings, which were showcased in Discover magazine as one of its top science stories last year, are an object lesson in the necessity to evaluate data free of presumption or ideology.

leopard frog
Jeremy Feinberg, a doctoral candidate at the School of Environmental and Biological Sciences, discovered a new species of frog in the urban ponds of New Jersey and Staten Island, New York. It was originally thought to be a leopard frog, pictured here. Photography by Brian Curry

Frogs Afield
In the urban ponds of Staten Island, New York, and New Jersey, a new species of frog leapt to the attention of a team comprising scientists from Rutgers, the University of California, Los Angeles, the University of California, Davis, and the University of Alabama. Biologists had thought that the frog, because of its physical resemblance, was a variety of the leopard frog. But not so, according to Jeremy Feinberg, a doctoral candidate at the School of Environmental and Biological Sciences. He helped make the initial discovery while researching the steep drop in the population of leopard frogs in the urban wetlands of New York and New Jersey. The species, discovered through its unusual croaks and confirmed by genetic testing, has yet to be named.

Adding Insult to Injury
Obesity brings its share of health risks: cancer, heart attacks, diabetes. Now, the low self-esteem common among obese people can become a source of illness, too, according to Janet Tomiyama, an assistant professor in the Department of Psychology in the School of Arts and Sciences. Stigma­tization promotes the excess production of the steroid hormone cortisol, which can suppress the immune system and decrease bone production. Stigmatized women also suffer from excessive oxidative stress, a marker of aging cells.

Nothing to Fear But Fear Itself
Can we have a genetic predisposition to fear, even if a threat doesn’t exist? That’s one of the questions posited by Gleb Shumyatsky, an associate professor in the Department of Genetics in the School of Arts and Sciences. His team’s findings could lead to new treatment for people suffering from anxiety disorders, such as post-traumatic stress disorder, and the memories associated with them.

By altering memory-related genes in portions of a mouse’s brain responsible for registering fear—the amygdala—and those genes responsible for inhibiting excessive fear in order to react appropriately to danger—the prefrontal cortex—the researchers were able to manipulate the behavior of mice to both forget, or overlook, a source of fear and, in another experiment, to have the mice remain fearful. Shumyatsky says scientists have to continue the hunt for molecules in the brain that govern specific memories and behaviors so that therapies and drugs can be developed to treat anxiety disorders.

Organ Protection
A research team in the Department of Biomedical Engineering at the School of Engineering, working with Massachusetts General Hospital, has come up with a plan to protect the liver from toxic drugs, the most common among them being acetaminophen, by inhibiting a type of communication among cells. Drug-induced liver injury is the most common cause of acute liver failure in the nation and the top reason for abandoning drug development or withdrawing them from the market.

By targeting the liver’s “gap junctions,” hollow multimolecular channels that connect neighboring cells, the researchers discovered that the gap junctions spread immune signals from injured liver cells to surrounding undamaged cells, promoting inflammation and injury. Working with mice, the team identified a small-molecule inhibitor of liver gap junctions that protected the mice from injury and death, according to a report written by Martin Yarmush, the Paul and Mary Monroe Professor of Biomedical Engineering.

The Great Depression
Among the elderly, depression afflicts close to 7 percent of the population, often complicating medical conditions like congestive heart failure, diabetes, and arthritis. According to Ayse Akincigil GSNB’98, 04, an assistant professor in the School of Social Work in New Brunswick, African Americans receive far less diagnosis and treatment for depression from health care providers because services like psychotherapy are in short supply in poorer neighborhoods. A solution? Provide depression screening and access to care in low-income and minority neighborhoods.

A Cure for Children
Scientists at Rutgers believe they have discovered the cause of a rare degenerative childhood disease that results in slurred speech and an inability to walk and can even lead to premature death. The genetic disease, known as axtaxia-telangiectasia, or A-T, primarily attacks the cerebellum, the region of the brain responsible for coordination and equilibrium. Karl Herrup, chair of the Department of Cell Biology and Neuroscience in the School of Arts and Sciences, discovered that mice and people who died from A-T had a protein known as HDAC4, which regulates bone and muscle development, in the wrong place of the brain’s nerve cells. Instead of appearing in the cytoplasm, the protein developed in the nucleus where it attacked histones, proteins that protect the DNA. The discovery could eradicate A-T as well as help cure other diseases that attack the nervous system, such as Alzheimer’s.