Tag: Gene

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Cutting Carbohydrates From the Diet May Increase Longivity

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You may be able to extend your life and stay fit throughout your old age with a simple change of diet that switches on your “youth” gene.

Professor Cynthia Kenyon, whom many experts believe should win the Nobel Prize for her research into aging, has discovered that carbohydrates directly affect the genes that govern youthfulness and longevity.

By tweaking the genes of roundworms, she has been able to help them live up to six times longer than normal.
->The carbohydrates we eat directly affect two key genes that govern youthfulness and longevity
The genes that controlled aging in worms also do the same thing in rats and mice, probably monkeys, and there are signs they are active in humans, too. She found that turning down the gene that controls insulin in turn switches on another gene which acts like an elixir of life.

The Daily Mail reports:
“Discovering the … [first] gene has prompted the professor to ­dramatically alter her own diet, cutting right back on carbohydrates. That’s because carbs make your body produce more insulin (to mop up the extra blood sugar carbs ­produce) … so the vital second gene, the ‘elixir’ one, won’t get turned on.”

Source: Daily Mail October 26, 2010

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Study Finds That Exercise can Override ‘Fat Genes’

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New research reveals why you can no longer use the excuse that your “genes” are making you fat …

Just because someone has the genes does not mean that they will become overweight or obese, “Lifestyle such as physical activity can modify the effect.”

Researchers took a look at 12 genetic variants known to increase the risk of obesity, and then tracked the physical activity levels of more than 20,000 people. They determined that physical activity can reduce the genetic tendency toward obesity by 40 percent.

Even being active just 30 minutes a day proved to be a good start in reducing the effects of the genes.

USA Today reports:
“U.S. experts say the study adds to the data on the importance of exercise for weight control. ‘This is more evidence that behavior can modify genetic predisposition,’ says Tim Church, director of preventive medicine research at the Pennington Biomedical Research Center in Baton Rouge.”

Source: USA Today August 31, 2010

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Antibody ‘Fixes Internal Bleeds’

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Scientists say they have discovered an antibody that could minimise the major internal bleeding seen in traumas like bullet wounds and car crashes.
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The team at Oklahoma Medical Research Foundation (OMRF) has discovered that a protein called histone is responsible for much of the damage.

They say they have found a specific type of antibody that can block the ability of histone to cause damage.

They say it could lead to new ways to treat diseases and serious injuries.

‘Life threatening’
Writing in the journal, Nature Medicine, the OMRF researchers found that when mice had a bad blood stream infection (sepsis), their blood contained high levels of histones.

They checked this in primates and humans and found the same result.

The histone protein normally sits in the nucleus of a cell, packed around the strands of DNA.

It regulates the DNA, causing it to fold and form the characteristic double helix.


Bullet wounds often lead to severe internal bleeding
When the cell is damaged by injury or disease, the histone is released into the blood system where it begins to kill the lining of blood vessels, causing damage, the OMRF researchers said.

This, they believe, results in uncontrolled internal bleeding and fluid build-up in the tissues, which are life threatening.

Dr Charles Esmon, of OMRF who led the research, said: “When we realised that histones were so toxic, we immediately went to work looking for a way to stop their destructive tendencies.”

Mouse antibody
Marc Monestier, a colleague at Temple University in Philadelphia, had already discovered a specific type of antibody known as a monoclonal antibody that could block the histones.

It had been observed that patients with auto-immune diseases make antibodies to the proteins in their cell nuclei but it was not known why.

This antibody came from a mouse with an auto-immune disease.

The OMRF team have tested the antibody in mice with sepsis and it does stop the toxic effects of the histones and they recover, the researchers say.

They now want to test it in primates and eventually humans.

Dr Esmon said histones were similar in all mammals because they were such basic building blocks.

So a mouse antibody should work equally well in a human.

He said: “We think it was an adaptation during evolution.

“Millions of years ago, when people and animals got ill, they did not die of heart attacks or car accidents they died of infectious diseases.

“Their immune systems went into overdrive throwing everything at it and we believe the histones in the cell nucleus, part of the basic building blocks of life, were the last resort.”

Dr Stephen Prescott, president of OMRF, said: “These findings offer some clues as to why people suffering from one traumatic injury often experience a catastrophic ‘cascade’ of secondary traumatic events.

“If we can figure out how to control the initial injury, perhaps that will stop the domino effect that so often follows.”

Source: BBC News: 26th.Oct.’09

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Oxidative Stress Extends Lifespan

Scientists at the University of California, San Diego claim to have identified a mechanism of oxidative stress that prevents cellular  damage.

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“We may drink pomegranate juice to protect our bodies from so-called ‘free radicals‘ or look at restricting calorie intake to extend our lifespan,” said Dr Trey Ideker, chief of the Division of Genetics in the Department of Medicine at UC San Diego’s School of Medicine and professor of bioengineering at the Jacobs School of Engineering.

“But our study suggests why humans may actually be able to prolong the aging process by regularly exposing our bodies to minimal amounts of oxidants,” Ideker added.

Reactive oxygen species (ROS), ions that form as a natural byproduct of the metabolism of oxygen, play important roles in cell signalling. However, due to environmental stress like ultraviolet radiation or heat or chemical exposure the ROS levels can increase dramatically, resulting insignificant damage to cellular damage to DNA, RNA and proteins, cumulating in an effect called oxidative stress.

The scientists claim to have discovered the gene responsible for this effect.

One major contributor to oxidative stress is hydrogen peroxide. While the cell has ways to help minimize the damaging effects of hydrogen peroxide by converting it to oxygen and water, this conversion isn’t 100 percent successful.

During the study, the researchers designed a way to identify genes involved in adaptation to hydrogen peroxide.

To figure out which genes might control this adaptation mechanism, the team ran a series of experiments in which cells were forced to adapt while each gene in the genome was removed, one by one, covering a total of nearly 5,000 genes.

They identified a novel factor called Mga2, which is essential for adaptation.

“This was a surprise, because Mga2 is found at the control point of a completely different pathway than those which respond to acute exposure of oxidative agents,” said Ideker.

“This second pathway is only active at lower doses of oxidation,” Ideker added.

“It may be that adaptation to oxidative stress is the main factor responsible for the lifespan-expanding effects of caloric restriction,” said Ideker.

“Our next step is to figure out how Mga2 works to create a separate pathway, to discover the upstream mechanism that senses low doses of oxidation and triggers a protective mechanism downstream.”

Click to see : Extend Your Life By Eating Right

Sources: :The study is published in PLoS Genetics.

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Dengue Virus Growth Protein Identified

A TEM micrograph showing Dengue virus virions ...
Image via Wikipedia

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By silencing genes one by one, scientists have identified dozens of proteins that help the dengue fever virus to grow and spread among  mosquitoes and humans. The research paves the way to potentially prevent or treat the disease, which infects millions worldwide every year.

Dengue is a mosquito-borne illness that can cause debilitating sickness and death. “Dengue is a nasty disease, and right now, there is no treatment for it and no way to prevent it,” said Mariano Garcia-Blanco, professor of molecular genetics and microbiology at Duke University Medical Centre (DUMC) and study co-author.

“But if we can find a weakness in the virus, we can design a strategy to fight it. This study has helped us identify some gaps in dengue’s armour,” he said.

Almost half the people in the world are vulnerable to the dengue virus, says the World Health Organisation. Public health officials are worried because dengue appears to be popping up in places where it has rarely appeared before. It may be fuelled by global warming.

Garcia-Blanco, used RNA interference (RNAi) to unlock dengue’s secrets. RNA interference is a normal biological process cells use to turn gene expression on or off depending upon which gene products, or proteins, are needed at any given moment.

“That very same system proved to be the perfect investigative tool for our study,” said Garcia-Blanco.

Garcia-Blanco and colleagues in Duke’s RNAi facility were able to knock down gene function in fruit fly cells infected with a strain of the dengue virus known as DENV-2.

Silencing one gene at a time allowed researchers to pinpoint which genes, or host factors, were essential to viral growth and which ones were not.

They used fruit flies as a model because the genetic tools needed for the same work in mosquitoes have not been developed as yet. The process yielded 116 host factors that appeared to be important for successful dengue infection in fruit flies.

In testing several of these host factors in mosquitoes at Johns Hopkins University, researchers subsequently discovered that at least one – and possibly a second – was necessary for dengue infection to occur in the insects, said a DUMC release.

Sources: The Times Of India

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