About 25 percent of Arab adults in Detroit reported abuse after 9/11
One quarter of Detroit-area Arab Americans reported personal or familial abuse because of race, ethnicity or religion since 9/11, leading to higher odds of adverse health effects, according to a new study.
Muslim Arabs also reported higher rates of abuse than Christians, says lead author Dr. Aasim Padela, a Robert Wood Johnson Foundation Clinical Scholar in the Department of General Medicine and clinical instructor in the Department of Emergency Medicine.
Padela says those who reported abuse showed a higher probability of having psychological distress, lower levels of happiness and poorer perceptions of health status.
What’s disturbing about the findings is that residents in Greater Detroit live in a large, well-established Arab community, where they might be expected to be protected from abuse, Padela says. Most of the respondents also had access to health insurance.
“Negative associations of perceived post-9/11 abuse or discrimination might be much worse in less concentrated Arab populations within the United States,” Padela says.
Approximately 490,000 Arabs reside in Michigan, and more than 80 percent of those live in metro Detroit’s Wayne, Oakland and Macomb counties. Arabs are the third largest ethnic population in Michigan, with a history dating back multiple generations. This community is the largest concentration of Arabs outside of the Middle East.
Padela and co-author Dr. Michele Heisler, associate professor of internal medicine and of health behavior and health education in the School of Public Health, used data from a face-to-face survey of Arab Americans administered in 2003.
This is the first representative, population-based investigation of the health and psychological impacts of Sept. 11 on Arabs and Muslims living in the United States, the researchers say.
The research was published online in the American Journal of Public Health.
— Mary Masson, UMHS Public Relations
The past matters to plants, researchers say
It’s commonly known that plants interact with each other on an everyday basis: they shade each other out or take up nutrients from the soil before neighboring plants can get them. Now, U-M researchers have learned that plants also respond to the past.
Emily Farrer, Deborah Goldberg and Aaron King modeled four years of population fluctuations in four species common to the Michigan dry sand prairie to determine how plants interacted with each other. They found that plants tended to compete, or negatively affect one another, over the summer, fall and spring; but interestingly the researchers also found that the more crowded together plants were in one growing season, the more their growth was enhanced the following year.
“For example, if a species had a large, dense population a year ago, this would promote current population growth, even though the plants are currently competing,” says Farrer, a graduate student in the Department of Ecology & Evolutionary Biology.
These time-lagged interactions may be due to effects from plant litter, Farrer says. After plants die back over the winter, the dead plant material starts to decompose, releasing nutrients that encourage plant growth. The litter layer also holds in soil moisture, a boon to plants struggling to survive in the dry environment.
The positive effect also may be due to the fact that the plants are perennial and can bank resources in below-ground roots and rhizomes until the following year, when they can be drawn upon to boost growth.
Goldberg is professor and chair and King is an assistant professor in the Department of Ecology and Evolutionary Biology.
The research appears in the February issue of The American Naturalist.
— Nancy Ross-Flanigan, News Service
Study examines how water forms where Earth-like planets are born
In a study that helps to explain the origins of water on Earth, U-M astronomers have found that water vapor can form spontaneously in habitable zones of solar systems, and that it develops into a protective layer that shields other water and organic molecules from harmful stellar radiation.
Organic molecules such as sugars and amino acids are the precursors to life.
“When you’re close to a star, the radiation is destructive to most molecules. But we were able to prove that water could form quickly enough to shield itself and other molecules from that radiation,” says Ted Bergin, an associate professor in the Department of Astronomy.
Bergin and Thomas Bethell, a postdoctoral astronomy researcher, conducted a computational analysis to come to this conclusion.
They determined that the series of chemical reactions necessary for water vapor to be created only are activated at temperatures higher than 300 degrees Kelvin (which is about 80 degrees Fahrenheit.) These temperatures only are present relatively close to a star — in the areas where terrestrial planets such as Earth would form. Out farther, at Jupiter’s distance, the gasses are too cold for water vapor to form.
Once the water vapor starts to form, the scientists found, it forms fast enough to build a shell similar to Earth’s ozone layer, which acts like an umbrella to protect the life below it from solar radiation. Not only does this astronomical “ozone layer” of water vapor protect other water molecules behind it, it would also shelter organic molecules.
Conceivably, some of this water and organic matter could be incorporated into nascent, Earth-like worlds.
The findings are published in the Dec. 18 edition of Science.
— Nicole Casal Moore, News Service
Immune cell activity linked to worsening COPD
A new study links chronic obstructive pulmonary disease, or COPD, with increased activity of cells that act as sentinels to activate the body’s immune system.
U-M and Veterans Affairs research adds to growing awareness of the immune system’s role in COPD, a serious, progressive lung disease that affects more than 12 million Americans with wheezing, shortness of breath, chest tightening and other symptoms. Understanding immune factors is key if doctors are to find better ways to detect and treat the disease early when patients might benefit most, believe some COPD researchers.
Nearly all people diagnosed with COPD have emphysema or chronic bronchitis or most commonly, both conditions. COPD is the fourth leading cause of death in the United States. Most people with COPD are smokers or former smokers.
“We found that dendritic cells, a type of immune cell that initiates immune responses, are in the lung interacting with lymphocytes, and that these dendritic cells seem to get more active as the disease goes on. If we could alter or stop their action, perhaps we could stop the disease from progressing,” says the study’s senior author Dr. Jeffrey Curtis, professor of internal medicine at the Medical School and chief of the pulmonary and critical care medicine section at the VA Ann Arbor Healthcare System.
Lung damage occurs well before people with COPD are aware of symptoms. By the time they seek medical help, the destructive forces of chronic lung inflammation often have taken a heavy toll. Immune cells in repetitive overdrive play a key role in that inflammation response, COPD researchers increasingly believe.
Additional U-M authors are Dr. Fernando Martinez, MeiLan Han, Theresa Ames, Stephen Chensue, Jill Todt, Douglas Arenberg, Catherine Meldrum, Christi Getty and Lisa McCloskey.
The study appears in the Dec. 15 issue of the American Journal of Respiratory and Critical Care Medicine.
— Anne Rueter, UMHS Public Relations
Molecular chaperone keeps bacterial proteins from slow-dancing to destruction
In new research, scientists at U-M and Howard Hughes Medical Institute have discovered how a protein chaperone called HdeA, which helps protect bacteria like the notorious Escherichia coli from the ravages of stomach acid, saves energy while keeping proteins from forming destructive clumps.
Proteins in disease-causing bacteria like E. coli unfold when they land in stomach acid after being accidentally ingested by humans and other animals. This unfolding stops the proteins from working and could spell doom for the bacteria if the chaperone HdeA didn’t step in. HdeA works by binding very tightly to the unfolded proteins while the bacteria are in the stomach. By attaching to the bacterial proteins, the chaperone stops them from tangling like slow-dancing teens, which could kill the bacteria.
The researchers discovered how HdeA is then able to let go of the unfolded proteins as the bacteria pass into the small intestine so that the proteins refold instead of clumping together.
“HdeA uses a unique timed-release mechanism,” says postdoctoral fellow Tim Tapley, who spearheaded the work. “If the proteins were released all at once they would likely clump together, killing the bacteria. What we found instead is that the chaperone HdeA lets go of them gradually, making it more likely that they fold back up into their proper form than clump together.”
While most molecular chaperones consume large amounts of cellular energy in order to function, HdeA instead taps energy freely available in its living environment.
Tapley and James Bardwell, professor of molecular, cellular and developmental biology and of biological chemistry, were assisted by research specialist Sumita Chakraborty, associate professor Ursula Jakob and Titus Franzmann, a postdoctoral fellow in the lab of Stefan Walter.
The research is described in a paper published online in the Proceedings of the National Academy of Sciences.
— Nancy Ross-Flanigan, News Service
