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Scholarship & Creative Work
Health choices predict cancer survival, U-M study finds

Head and neck cancer patients who smoked, drank, didn't exercise or didn't eat enough fruit when they were diagnosed had worse survival outcomes than those with better health habits, according to a new study from the Comprehensive Cancer Center.

"While there has been a recent emphasis on biomarkers and genes that might be linked to cancer survival, the health habits a person has at diagnosis play a major role in his or her survival," says study author Sonia Duffy, associate professor of nursing at the School of Nursing, research assistant professor of otolaryngology at the Medical School, and research scientist at the Veteran's Administration Ann Arbor Healthcare System.

Each of the factors independently was associated with survival. Results of the study appear online in the Journal of Clinical Oncology.

The researchers surveyed 504 head and neck cancer patients about five health behaviors: smoking, alcohol use, diet, exercise and sleep. Patients were surveyed every three months for two years then yearly after that.

Smoking was the biggest predictor of survival, with current smokers having the shortest survival. Problem drinking and low fruit intake were associated with worse survival, although vegetable intake was not. Lack of exercise also appears to decrease survival.

Complicating matters is that many of these health behaviors are inter-related. For example, smokers might also be heavy drinkers, making it more difficult to quit. It's not enough, Duffy points out, to refer someone to a smoking- cessation program if alcohol is a major underlying problem.

In addition, previous research has associated many of these health behaviors with preventing cancer. In the current study, a third of the patients reported eating fewer than four servings of fruit per month. Nutrition experts recommend two servings of fruit per day.

Additional authors: David Ronis, associate research scientist, School of Nursing; Dr. Scott McLean, Henry Ford Health System; Karen Fowler, research associate; Dr. Stephen Gruber, associate professor of internal medicine, human genetics and epidemiology, Medical School and School of Public Health; Dr. Gregory Wolf, professor of otolaryngology, Medical School; and Dr. Jeffrey Terrell, associate professor of otolaryngology, Medical School.

Yeast biology yields insights into human knowledge expansion

How does human knowledge expand over time? Intriguing as the question is, it's not easy to investigate, due to the difficulty of measuring knowledge and its spread.

But by analyzing three decades of discoveries about baker's yeast — an organism extensively studied for insights into the workings of genes and proteins — university researchers have revealed interesting patterns in the proliferation of scientific understanding. Their findings, published online in the open-access journal PLoS Computational Biology, suggest ways to make scientific endeavors more productive.

In recent decades, scientists significantly have furthered their knowledge of yeast biology by studying interactions among the organism's 6,000 or so genes.

In the current study, Jianzhi Zhang, an associate professor of ecology and evolutionary biology, and his former graduate student Xionglei He, now at Sun Yat-sen University in Guangzhou, China, explored the explosive growth of this research field.

A surprising finding emerged when Zhang and He looked at the productivity of individual researchers involved in yeast studies. Although research in the life sciences increasingly is done in large teams, "We found that scientists who engage in large collaborations tend to have smaller contributions per scientist than those who work in smaller groups," Zhang says.

Could that be because large groups typically include many junior scientists, whose productivity is lower than that of more established researchers? Zhang and He thought so at first. "But when we considered senior authors only, we still found lower productivity," says Zhang, who believes that large group collaborations are simply less efficient than small teams.

Signaling pathway gives clues to treating Tylenol toxicity

Taking acetaminophen, commonly known by the brand name Tylenol, can turn into too much of a good thing if, in the course of treating backaches and arthritis, it damages liver cells. Warning labels indicate taking more than the recommended dose may cause liver damage.

University researchers have found a new pathway in the immune system to distinguish between the system's response to infection vs. cellular injury, such as liver cells damaged by drug toxicity.

The findings, released online March 5 and published in Science, point to possible genetic control and treatment of acetaminophen overdose, the most common drug overdose-related hospitalization in the United States. Plus, it has implications for genetic control and treatment of other types of cell injuries, including trauma and tissue damaged by heart attacks or strokes.

The study was led by Dr. Yang Liu, director of the Division of Immunotherapy in the Department of Surgery at the Medical School.

While it is possible that some people are sensitive to acetaminophen overdose due to genetic defects, the study suggests another tool for treating acute liver damage caused by drug toxicity.

In addition to Liu, director of the Cancer Immunology Program of the U-M Comprehensive Cancer Center, the study was led by Dr. Pan Zheng, associate professor in the departments of Surgery and Pathology at the Medical School.

Other co-authors are Dr. Guo-Yun Chen, research fellow in the U-M Department of Surgery; and Jie Tang, Institute of Biophysics, Chinese Academy of Science, Beijing.

Scientists have better understanding of blood sugar control

Scientists are closer to understanding which proteins help control blood sugar, or glucose, during and after exercise. This understanding could lead to new drug therapies or more effective exercise to prevent Type 2 diabetes and other health problems associated with having high blood sugar.

Insulin resistance happens when insulin produced by the body doesn't properly stimulate the transport of glucose into the cells for energy. Too much glucose in the bloodstream can cause a host of medical problems, including Type 2 diabetes, says Gregory Cartee, professor at the School of Kinesiology.

Insulin and muscle contractions are the two most important stimuli to increase glucose transport into muscle cells. Cells then use the glucose for energy. However, scientists aren't entirely sure how this works.

Cartee and colleague Katsuhiko Funai, a graduate student researcher in kinesiology, looked at how two different proteins believed to be important in stimulating glucose transport react to two different enzymes also related to glucose transport. The goal of the study was to understand the contribution of the two proteins, AS160 and TBC1D1, in skeletal muscle stimulated by insulin.

"We're trying to rule out or rule in which proteins are important with exercise," Cartee says.

The study will appear in an upcoming print edition of the journal Diabetes. For an advance online copy, go to

Professor recording Bach's complete organ works

James Kibbie, professor of organ at the School of Music, Theatre & Dance, is undertaking a three-year project to record the complete organ works of Johann Sebastian Bach.

Kibbie is recording some 270 extant Bach organ works, totaling more than 18 hours, on original 18th-century organs in Germany. Bach played most of the organs and in some cases helped to design them. The university will make these recordings available free of charge as Internet downloads, marking the first time the complete canon of Bach organ works will be available through the Internet. The Web site will also feature information on the organs, the music, and U-M's Historic Organ Tours.

During the 2007 phase of the project, Kibbie recorded the Leipzig Chorales, the Kirnberger Chorales, and a variety of free works on the historic Gottfried Silbermann organs in the Hofkirche in Dresden and the Georgenkirche and Marienkirche in Rotha.

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