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Scientists to Study Ozzy Osbourne’s Genome

Ozzy Osbourne’s genome has been sequenced, in hopes that scientists can figure out how the notoriously self-destructive rocker is still alive.

Although the 61-year-old Osbourne has been sober for several years, Ozzy spent most of his adulthood engaging in behavior typical of a rock star musician. He was heavily into drinking and drugs for 40 years. He broke his neck on a quad bike. He died twice in a chemically induced coma. He walked away from a tour bus accident without a scratch after it was hit by a plane. His immune system was so compromised by his lifestyle he once received a positive HIV test, until it was proved to be a false positive. Yet here he is – Ozzy is alive and well.

Recently, Ozzy became a member of an elite group of people when he had his full genome sequenced. In addition to giving Osbourne information that could help prevent diseases, it is hoped the results will provide insights into the way drugs are absorbed into the body.

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New Genetic Factors Identified in Successful Aging of Amish Population

Avoiding disease, maintaining physical and cognitive function, and continuing social engagement in late life are considered to be key factors associated with what some gerontologists call “successful aging.”

First and foremost, let me strongly disagree here with those gerontologists. I believe the term “successful aging” is absolutely intolerable. Just think about it. How on Earth can aging be somewhat successful? Aging brings diseases, mental incapacity and other deteriorating effects on the human body. We cannot call that successful under any circumstances.  So for the purpose of this article, we have replaced the term “successful aging” with “less destructive aging.”

While conducting studies of Amish families in Indiana and Ohio, a group of researchers led by William K. Scott, PhD, Professor of Human Genetics at the University of Miami Miller School of Medicine, began to notice that a significant number of people over age 80 in these communities demonstrated the three main factors associated with less destructive aging.

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Scientists Discover New Way to Detect and Fix DNA Damage

Researchers at Vanderbilt University, Pennsylvania State University and the University of Pittsburgh have discovered a new mechanism that detects and repairs a more common form of DNA damage called alkylation.
In a typical day, about one million bases in the DNA of a human cell are damaged. These lesions are caused by a combination of normal chemical activity within the cell and exposure to radiation and toxins coming from environmental sources including cigarette smoke, grilled foods, UV rays and industrial waste. These lesions cause structural damage to the DNA molecule, and can dramatically alter the cell’s way of reading the information encoded in its genes. Luckily, repairing damage and maintaining the integrity of its DNA is one of the cell’s highest priorities. 

As cells age however, the DNA repair process can no longer keep up with ongoing DNA damage. The cell then suffers one of three possible outcomes:
* An irreversible state of dormancy, known as senescence (http://en.wikipedia.org/wiki/Senescence)
* Cell suicide, also known as apoptosis (http://en.wikipedia.org/wiki/Apoptosis) or programmed cell death
* Cancer
When cells become senescent, alterations in their gene regulation cause them to function less efficiently, which inevitably causes disease. The DNA repair ability of a cell is vital to its normal functioning and to the health and longevity of the organism. Many genes that are shown to influence lifespan are associated with DNA damage repair and protection.

“There is a general belief that DNA is ‘rock solid’ – extremely stable,” said Brandt Eichman (http://structbio.vanderbilt.edu/faculty/eichman.php), associate professor of biological sciences at Vanderbilt, who directed the project. “Actually DNA is highly reactive,” he was quoted as saying.
According to the Vanderbilt study, when a DNA base becomes alkylated, it forms a lesion that distorts the shape of the molecule enough to prevent successful replication. Human cells contain a single glycosylase (http://en.wikipedia.org/wiki/DNA_glycosylase), named AAG that repairs alkylated bases. It’s specialized to detect and delete “ethenoadenine” bases, which have been deformed by combining with highly reactive, oxidized lipids in the body.

“It’s hard to figure out how glycosylases recognize different types of alkylation damage from studying AAG since it recognizes so many. So we have been studying bacterial glycosylases to get additional insights into the detection and repair process,” said Eichman.
That is how they discovered the bacterial glycosylase AlkD with its unique detection and deletion scheme. “All the known glycosylases work in basically the same fashion: hey flip out the deformed base and hold it in a special pocket while they excise it. AlkD, by contrast, forces both the deformed base and the base it is paired with to flip to the outside of the double helix.”

“Understanding protein-DNA interactions at the atomic level is important because it provides a clear starting point for designing drugs that enhance or disrupt these interactions in very specific ways,” says Eichman. “So it could lead to improved treatments for a variety of diseases, including cancer.”

So there is a vast body of evidence that correlates DNA damage to death and disease. As indicated by the findings of the Vanderbilt study, increasing the activity of some DNA repair enzymes could cause a decrease in the rate of cell damage which would result in adding many healthy and disease-free years to our aging population.
Read about the DNA Repair study: (http://news.vanderbilt.edu/2010/10/newly-discovered-dna-repair-mechanism/)

Maria Konovalenko 
SCIENCE FOR LIFE EXTENSION FOUNDATION 
http:/mariakonovalenko.wordpress.com/ 
maria.konovalenko@gmail.com

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