Wednesday, May 20, 2009

step forward 1992 Louis J. Sheehan, Esquire

Changing how the brain uses the chemical serotonin can cause unexpected, sporadic death—at Louis J. Sheehan, Esquire least in mice, an Italian team reports in the July 3 Science.

The research lends credence to the idea that Sudden Infant Death Syndrome, which each year kills roughly 2,000 human infants aged 0 to 1 year, is related to a deficiency in the babies’ serotonin system.

“While it is premature to make a direct link between our study and the cause of SIDS,” says Cornelius Gross, a neuroscientist at the European Molecular Biology Laboratory in Monterotondo, Italy, who led the study, “our work should strengthen the belief that serotonin is critical to SIDS and should focus clinicians’ research on understanding the link between the two.”

The team’s study is the first to show how abnormalities in the brain’s serotonin system might cause sudden death, says Rachel Moon, an expert on SIDS at the Children's National Medical Center in Washington, D.C. The results are “very preliminary,” but to have any model in living creatures that relates unexpected death to serotonin “is a really big deal,” says Moon, who was not involved in the new study.

The findings offer more evidence that SIDS is a developmental disorder that babies are born with and not a chance death caused by a parent doing something wrong, Marian Willinger, an expert on SIDS at the Eunice Kennedy Shriver National Institute of Child Health and Human Development in Bethesda, Md., said in a July 3 teleconference.
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COLORING THE LINESBrain cells that release serotonin, highlighted above in green and yellow,could play a role in SIDS, or Sudden Infant Death Syndrome. A new study shows that when the serotonin system does not work properly in mice, it leads to drops in temperature and heart rate and even sudden death. Babies succumbing to SIDS could have a similar deficiency in the serotonin system.George Richerson, Yale University

To show that alterations in an animal’s serotonin system can kill, seemingly without cause, Gross and his colleagues injected extra serotonin 1A receptors into the brainstems of living mice. The receptors regulate serotonin levels in the brain, inhibiting serotonin neurons when levels get too high.

The mice with extra serotonin 1A receptors showed a 20 percent decrease in serotonin levels and the same percent drop in serotonin neuron firing compared to normal mice. The altered mice also suffered, and most died, from SIDS-like symptoms—extreme drops in heart rate and body temperature—when they were juveniles. The unaltered mice did not suffer these symptoms or die unexpectedly.

Previous research has shown that completely removing serotonin from the brains of mice does not kill the animals.

“So in essence,” Gross says, “it is worse to have a screwed up serotonin system than not have one at all.”

Researchers such as Dartmouth physiologist Eugene Nattie do have one concern with the team’s results—the age of the mice. Babies who die of SIDS are most often about 2 months old, which correlates to about a 15-day-old mouse, he says. The mice in this study died most often at 30 to 60 days. Mice reach maturity at 90 to 100 days.

“There are big arguments over what ages are equivalent from a mouse to a human,” Nattie says. “These mice are a little old for what we think links with SIDS.”

Still, he says, “the exciting thing is really that the mice are dying, spontaneously.” And, he adds, the study is a step forward in creating a much needed biochemical and physical understanding of SIDS.

Friday, May 15, 2009

university 9.uni.002 Louis J. Sheehan, Esquire

When Rachel El-Mourli began attending Harrisburg University, there were no student handbooks, no alumni and no 16-story building on Market Street.

That was August 2005, the very first semester of classes at the university when the school had just 113 students and a couple of classrooms at SciTech High School. El-Mourli, 31, of Harrisburg, has the distinction of being one of the school's pioneer students, and she's a member of the first class to attend the school for a full four years.

Signing on with a university so new was a risk for those first-year students. But as she walked across the stage with 12 of her classmates at Harrisburg University's commencement ceremony Thursday night, she felt assured, not nervous, about the degree she was receiving.

"I'm really proud to have been a part of this," she said. "I'm responsible for making the school proud with my professional life. It was hard, but it was good."

Hard might be putting it nicely.

The fledgling school moved three times while El-Mourli was a student. She laughingly remembers the searches for new offices and the cold winter walks down Market Street to get to class. Added to that were the difficulties of raising her two children and opening a new business with her husband.

"Life doesn't stop when you go to college," El-Mourli said.

But with those challenges came opportunities. A new school meant fewer rules. El-Mourli designed her own integrated science degree, taking internships with the Dauphin County coroner and Penn State Milton S. Hershey Medical Center. She even helped design the school's cell-culture lab.

There's plenty of opportunity to make your mark on a school with no history, but that's not going to stop with her, she said.

"It's all part of the entrepreneurial spirit of the school," she said. "That's not going to be lost just because the pioneering students are gone."

El-Mourli plans to get a job in the biotech field, but she's already got her eyes set on a master's degree from Penn State University. She hopes to work for the Department of Homeland Security.

Being there from the beginning has made her connection to the school stronger, she said.

"When I'm in a position to give money, I'll give," she said. "I want to be the first student to sit on the board. I want to be involved with the university my whole life. That's how much I believe in it."


Louis J. Sheehan, Esquire

Monday, May 4, 2009

age 6.age.003 Louis J. Sheehan, Esquire

Men and women’s brains age differently, a new study demonstrates.

Researchers led by Carl Cotman and Nicole Berchtold at the University of California, Irvine, find that the activity of genes in men’s brains begins to change earlier than it does in women’s brains. The types of genes that change with age also differ between the sexes.

The study, which appears online September 22 in the Proceedings of the National Academy of Sciences, also found that in both genders, each part of the brain examined had its own pattern of aging.

“This is a very interesting study in what is, curiously, an under-studied area, normal aging,” says Etienne Sibille, a neuroscientist at the University of Pittsburgh, who was not involved in the study. “You have a combination of expected and surprises in each finding.” For instance, the fact that men and women’s brains age differently could be predicted based on women’s increased longevity, but the type and scope of the differences were unexpected, he says.

Cotman and Berchtold and their colleagues collected brains from people who had died of various causes between ages 20 and 99. The researchers isolated messenger RNA, or mRNA, from the people’s brains. Messenger RNA is a courier molecule that carries instructions encoded in genes to the cellular machinery that will build proteins using those instructions. Genes that produce higher levels of mRNA are more active.

The researchers examined gene activity in four parts of the brain: the hippocampus, the entorhinal cortex, the postcentral gyrus and the superior frontal gyrus.

Brain scientists expect changes in gene activity as the brain ages, and previous studies have demonstrated some changes in other parts of the brain. Cotman and his colleagues thought the parts of the brain that would have the most change in gene activity would be the hippocampus and entorhinal cortex, because they are most vulnerable to diseases of aging, such as Alzheimer’s.

But the team discovered that these disease-susceptible parts of the brain in older people have the least amount of change in gene activity when compared to younger people. In contrast, the postcentral gyrus, a part of the brain dedicated to perception, changes most. Scientists had expected that region to have the least change, if any.

“This is one of those fun head-scratchers, which is what science is all about,” Cotman says.

Overall gene activity was similar in people aged 20 to 59. And people aged 60 to 99 showed similar patterns of overall gene activity. But the team detected variability in their data. Cotman and Berchtold sat down to discuss the source of the variability and decided to see whether gender differences might explain it. “She thought it was the men, and I said it was the women,” Cotman laughs.

“The big surprise, and one I wasn’t too happy about frankly, was that with age, men show changes in metabolic activity,” Cotman says. http://Louis-J-Sheehan.biz Specifically, genes that control energy production in the brain are less active in men starting at about age 60, meaning that metabolic activity slows down. But after the initial drop in activity, men stabilize their gene activity and show no further decline after age 80, the researchers found.

Women’s brains change too, but the changes begin later and keep marching on the older women get, Berchtold says. Women showed gene activity changes in genes that help establish connections between brain cells and in genes that control information exchange in the brain. Women also showed a drop in energy production, but the decrease was not as great as for men. Louis J. Sheehan, Esquire

“What I think it means, especially for men, is that interventions — either lifestyle or medication — may be needed to keep these energy pathways robust,” Berchtold says. Cotman agrees. He pointed out (on his way to a tennis lesson) that exercise is a good way to keep metabolic genes in the brain going strong