The memories you want to forget are the hardest ones to lose

CHAPEL HILL – Painful, emotional memories that people would most like to forget may be the toughest to leave behind, especially when memories are created through visual cues, according to a new study by the University of North Carolina at Chapel Hill.

“When you’re watching the news on television and see footage of wounded soldiers in Iraq or ongoing coverage of national tragedies, it may stick with you more than a newspaper headline,” said the study’s lead author, Keith Payne, an assistant professor of psychology in the College of Arts and Sciences.

It is adaptive to be able to intentionally forget neutral events such as wrong directions, a friend’s outdated phone number or a switched meeting time. Intentional forgetting helps update memory with new information, Payne said.

But Payne and former psychology graduate student Elizabeth Corrigan found that even “mild” emotional events, like getting a bad grade on a test or a negative comment from a coworker, can be hard to forget. Their study, “Emotional constraints on intentional forgetting,” appears in the September 2007 print issue of the Journal of Experimental Social Psychology.

When people are trying to intentionally forget information, they need to mentally segregate that information and then block off the information they don’t want to retrieve, Payne said.

Emotion undermines both of those steps. “You make a lot of connections between emotional events and other parts of your life, so it might be difficult to isolate them. As far as blocking retrieval of an unwanted event, emotion makes events very salient and therefore highly accessible,” Payne said.

Their results contrast with previous studies of emotional events and intentional forgetting, but those studies used emotion-laden words as stimuli, like “death” and “sex.” The UNC study took a new approach, asking 218 participants to react to photographs instead of text.

“The word ‘murder,’ for instance, may or may not make you afraid, but if you see a graphic, violent picture, it may be powerful enough emotionally to change the way you feel,” Payne said.

The researchers found that their subjects could not intentionally forget emotional events as easily as mundane ones. They also found that both pleasant and unpleasant emotional memories were resistant to intentional forgetting.

The UNC findings contribute to understanding the ways that emotion constrains mental control and to the question of whether intentional forgetting can be helpful in coping with painful or traumatic experiences.

“Our findings add to accumulating evidence that emotion places limits on the ability to control the contents of the mind,” Payne said. “Our results suggest that even a relatively mild emotional reaction can undermine intentional forgetting. But this doesn’t necessarily mean that emotional memories can never be intentionally forgotten. If the motivation to forget is powerful enough, individuals might be able to overcome the effects of emotion by enlisting additional coping strategies.”

A different study would be needed to examine what treatment and coping strategies might be effective in helping people voluntarily forget an unwanted memory, he added.

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Web site: The study can be found online at http://www.sciencedirect.com.

Note: Payne can be reached on his cell phone (919) 951-9177 or by email payne@unc.edu. He will be in San Francisco at the American Psychological Association convention until Sunday, Aug. 19 but will be taking calls and checking email. After Aug. 19, Payne can be reached at (919) 962-2055 or by email.

College of Arts and Sciences contact: Kim Spurr, (919) 962-4093, spurrk@email.unc.edu
News Services contact: Clinton Colmenares, (919) 843-1991, clinton_colmenares@unc.edu

Contact: Clinton Colmenares
clinton_colmenares@unc.edu
919-843-1991
University of North Carolina at Chapel Hill

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Multicenter study nets new lung tumor-suppressor gene

BOSTON–Collaborating scientists in Boston and North Carolina have found that a particular gene can block key steps of the lung cancer process in mice. The researchers report in the journal Nature that LKB1 is not only a “tumor-suppressor” gene for non-small cell lung cancer in mice, it also may be more powerful than other, better-known suppressors. The study will be published on the journal’s Web site on Aug. 5 and later in a print version.

If further research shows LKB1 has a similar effect in human lung cells, it could influence the way non-small cell lung cancer is diagnosed and treated, says the study’s senior author, Kwok-Kin Wong, MD, PhD, of Dana-Farber, one of three institutions, along with Massachusetts General Hospital and the University of North Carolina School of Medicine, leading the work. If tumors with LKB1 mutations are found to be especially fast-growing, for example, patients with such tumors might be candidates for more aggressive therapy.

People born with defective versions of LKB1 often develop Peutz-Jeghers syndrome, which is marked by intestinal growths and an increased risk for certain cancers. Non-inherited mutations of the gene have been found in some lung cancers. This suggested that LKB1 normally thwarts tumors from forming. Mutated versions may be unable to act as a brake on cancer.

To find out, the investigators ran a series of experiments in mice with a defective form of a gene called Kras, which drives the formation and growth of lung cancer. They tracked the development of lung cancer in animals with mutated LKB1 and compared it to the experience of animals with abnormalities in either of two well-known tumor-suppressor genes.

They found that while Kras “cooperated” with the mutated tumor-suppressor genes to produce lung cancer, it cooperated even more strongly with mutated LKB1. “The LKB1-deficient tumors grew more rapidly and spread more frequently than the others, and comprised all three types of non-small cell lung cancer — squamous cell carcinoma, large-cell carcinoma, and adenocarcinoma — rather than just one or two,” Wong says. “This suggests that LKB1 plays a role at major stages of the tumors’ development: initiation, differentiation of normal lung cells into cancer cells, and metastasis.”

An examination of human non-small-cell lung tissue suggests LKB1 mutations play a role there as well. Of 144 samples analyzed, 34 percent of the lung adenocarcinomas and 19 percent of the squamous cell carcinomas contained abnormal versions of the gene, researchers report.

“We were surprised at how significant a role LKB1 mutations play in non-small cell lung cancer development in mice,” say Wong, who is also an assistant professor of medicine at Harvard Medical School. “This suggests there may be additional lung tumor-suppressor genes yet to be discovered. We’re currently examining whether these results apply to human lung cancers as well and, if so, how such information can improve treatment.”

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The lead author of the study was Hongbin Ji, PhD, of Dana-Farber. Other Dana-Farber co-authors include Dongpo Cai, PhD, Liang Chen, PhD, Pasi Janne, MD, PhD, Bruce Johnson, MD, Jussi Koivunen, MD, PhD, Danan Li, Mei-Chih Liang, PhD, Kate McNamara, Matthew Meyerson, MD, PhD, Samanthi Perera, PhD, Geoffrey Shapiro, MD, PhD, and Takeshi Shimamura, PhD. Other authors were based at Children’s Hospital Boston, Brigham and Women’s Hospital, Broad Institute of Harvard University and Massachusetts Institute of Technology, University of Tennessee Health Science Center, and the University of Texas Southwestern Medical Center.

The research was supported by the National Institutes of Health, the Sidney Kimmel Foundation for Cancer Research, the American Federation of Aging, the Joan Scarangello Foundation to Conquer Lung Cancer, the Flight Attendant Medical Research Institute, the Waxman Foundation, the Harvard Stem Cell Institute, and the Linda Verville Foundation.

Dana-Farber Cancer Institute (www.dana-farber.org) is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute.

Contact: Bill Schaller
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute

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Coarse particulate matter in air may harm hearts of asthma sufferers, UNC study finds

News Release

For immediate use May 9, 2007

CHAPEL HILL – Breathing air containing coarse particulate matter such as road or construction dust may cause heart problems for asthma sufferers and other vulnerable populations, according to a new study led by the University of North Carolina at Chapel Hill School of Public Health.

The researchers found that in people with asthma, a small increase in coarse particulate matter in outdoor air raised bad cholesterol and increased the count of inflammation-linked white blood cells, among other changes.

“This research was all done with study participants just being outside and breathing outdoor air,” said Dr. Karin Yeatts, research assistant professor of epidemiology at the UNC School of Public Health, a member of the UNC Center for Environmental Medicine, Asthma and Lung Biology, and the study’s principal investigator. “Our results indicate that susceptible people really need to pay attention to air pollution warnings and stay inside when the air pollution is bad. This is particularly the case for people with asthma.”

The study, published in the May 2007 issue of Environmental Health Perspectives, was a collaboration by researchers from the School of Public Health, the School of Medicine’s Center for Environmental Medicine, Asthma and Lung Biology and the U.S. Environmental Protection Agency (EPA).

The team found that when adult asthma sufferers were exposed to a one microgram per cubic meter increase in coarse particulate matter in ambient air their triglyceride levels increased by nearly five percent. Elevated levels of triglycerides have been shown to increase one’s risk of coronary heart disease. The amount of eosinophils in study participants’ blood also increased by 0.16 percent after exposure to the higher levels of coarse particulate matter. Eosinophils are a type of white blood cell created by the human body to fight infections, allergies and diseases like asthma among other things. Finally, the same increase in coarse particulate matter resulted in a three percent decrease in a measure of heart rate variability, the variation of the beat-to-beat intervals of the heart. A healthy heart has wide heart rate variability, while decreased variability can indicate stress or cardiac disease.

Surprisingly, there was no relationship between coarse particulate matter and rescue medication use, asthma symptoms, lung function or airway inflammatory markers, Yeatts said. However, 10 of the 12 adult asthmatics in the study were taking anti-inflammatory controller medication for their disease, and nine of the 12 had mild disease. It is possible that anti-inflammatory treatment mitigated the effects in their airways, or that adults with asthma are less susceptible to the effects of coarse particulate matter.

Study participants consisted of 12 adults between the ages of 21 and 50 with persistent asthma. All lived within a 30-mile radius of the study’s particulate matter monitor, located on the EPA Human Studies Facility at the Carolina campus. Each study participant took part in nine clinic visits: five the first week, and four spaced randomly over the subsequent six to 11 weeks. Data collection took place between September 2003 and July 2004. During the study, outdoor air levels of coarse particulate matter ranged between zero to 14.6 micrograms per cubic meter and did not exceed safety levels set by the EPA of 150 micrograms per cubic meter.

Other study authors include Lawrence Kupper, Alumni Distinguished Professor of biostatistics in the UNC School of Public Health; Dr. David Peden, director of the UNC Center for Environmental Medicine, Asthma and Lung Biology; Neil Alexis and Margaret Herbst, UNC Center for Environmental Medicine, Asthma and Lung Biology; Erik Svendsen, John Creason, James Scott, Lucas Neas, Robert Devlin and Ronald Williams of the EPA; and Dr. Wayne Cascio of Eastern Carolina University’s Brody School of Medicine.

School of Public Health contact: Ramona DuBose, (919) 966-7467 or ramona_dubose@unc.edu
News Services contact: Becky Oskin, (919) 962-8596 or becky_oskin@unc.edu

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