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When the World Trade Center towers began burning on Sept. 11, 2001, the estimated 15,000 to 20,000 people inside had to get out quickly. While most of the people escaped, nearly 3,000 perished, raising questions about the effectiveness of the evacuation plan.

Now researchers at Columbia University Health Sciences are leading a study of the evacuation procedures to identify strategies to improve mass evacuation of high-rise buildings under extreme conditions. The Columbia researchers, who are from the Department of Sociomedical Sciences and the Center for Public Health Preparedness at the Mailman School of Public Health, are collaborating with researchers at New York University and John Jay College of Criminal Justice. The initial phase of the three-year, $2.5 million study is being funded by the Centers for Disease Control and Prevention in collaboration with the Association of Schools of Public Health.

Led by Dr. Robyn Gershon, associate professor of sociomedical sciences at Mailman, the researchers will select and interview 200 people who were in the buildings, including office workers, building staff, police officers, firefighters, and Port Authority officials. The researchers will use the interviews to refine a questionnaire to be distributed to a random sample of 5,000 of the people who were in the buildings that day. The interviews and survey will evaluate what individual, organizational, and structural factors served as facilitators or barriers to evacuation.

Teams of researchers, survivors, and family members of the deceased workers will evaluate the interview and survey results to identify ways to reduce the loss of life in high-rise building catastrophes. Findings will be presented through a series of conferences open to the public at the New York Academy of Medicine.

The study's results may eventually lead to regulatory changes that could help improve evacuation procedures from high-rise structures, Dr. Gershon says.

A behavioral scientist who investigates occupational safety for high-risk work groups and bioterrorism, Dr. Gershon plans to apply a public health approach and analytical techniques to the World Trade Center evacuation study. To date, civil engineers have directed the few studies of high-rise building evacuation.

—Matthew Dougherty

Liver transplantation is the only cure for people with end-stage liver disease but the supply of cadaver livers is too small to meet the demand. In the United States last year, approximately 17,000 patients waited for livers while fewer than 5,000 cadaver livers were transplanted.

Liver scarcity has pushed surgeons to use livers from live donors as an alternative source. Adults can donate more than half of their livers because the organ, unlike others, can regenerate. But transplanting sections of a liver from one adult to another has been done only during the last four years and, thus, data on the risks and benefits for donors and recipients are limited.

Now Columbia University Health Sciences researchers are helping lead an approximately $20 million, seven-year study of the effectiveness of live donor liver transplants and optimal care for donors and recipients. The study, called the Adult to Adult Living Donor Liver Transplant Cohort Study, involves 10 universities and is funded by the National Institute of Diabetes and Digestive and Kidney Diseases, the Health Resources and Services Administration, and the American Society of Transplant Surgeons.

The national project will track a group of approximately 1,000 patients eligible for live donor liver transplantation, enrolling about 200 a year for five years, says study co-chair Dr. Jean Emond, T.S. Zimmer Professor of Reconstructive Surgery at P&S and chief of transplantation services at NewYork-Presbyterian Hospital.

The researchers will study factors that influence outcomes for donors and recipients and will compare the outcomes of patients with live donor liver transplantation to the outcomes of those who receive livers from cadavers. In addition to clinical issues, the researchers will investigate liver regeneration, liver cancer, and infectious hepatitis. Dr. Emond is a member of the four-person executive committee that directs the grant.

—Matthew Dougherty

Columbia University Health Sciences researchers and colleagues studying a mouse predisposed to Type II diabetes were able to stop the disease in the animal by reducing its production of a protein called Foxo1. The findings, published in the October Nature Genetics, provide a new understanding of the cause of the condition and suggest that drugs that reduce Foxo1 gene activity in humans could alleviate many of the problems caused by the disease.

Approximately 90 percent of people with diabetes have Type II, or adult-onset diabetes, which is a leading cause of death in industrialized countries. Type II diabetes develops because the pancreas loses its ability to manufacture insulin, cells in the body fail to respond to insulin, and the liver releases too much glucose. Glucose then builds up in the bloodstream and causes the complications of the disease.

When researchers, led by Dr. Domenico Accili, professor of medicine at P&S and at the Naomi Berrie Diabetes Center, reduced the production of Foxo1 by half, the level of glucose in the diabetic mice declined to normal levels.

The reduction in Foxo1 lowered glucose levels through two mechanisms, the researchers report. First, the liver reduced glucose production and second, beta cells in the pancreas regained their ability to make insulin, the hormone that tells cells to remove glucose from the bloodstream.

The results imply that two critical contributors to diabetes—increased glucose production and decreased insulin production—are intimately related to each other through Foxo1. Previously it was thought the two processes were independent abnormalities caused by another problem in diabetes, the resistance of muscle and fat cells to insulin.

The research also supports the emerging theory that an increase in glucose and a decrease in insulin are not simply the body's reactions to insulin resistance in fat and muscle, as previously thought. "Insulin resistance in fat and muscle is only half the story," Dr. Accili says. "The liver and beta cells are not passive bystanders in diabetes, but active participants."

—Susan Conova