Massage has beneficial Affect on Gene Activity: Reduces Muscle Inflammation

New research conducted at the McMaster University in Canada has indicated that apart from inducing deep relaxation, kneading sore muscles after a vigorous exercise can help them recover faster.

The scientists, through a series of experiments on young test subjects, have found that massaging sore muscles affected the activity of certain genes in the body. These genes were found to have a direct impact on reduced inflammation of the concerned muscles.

In fact, this "gene-stimulating" technique reportedly has the same effect on sore muscles that drugs like Ibuprofen or Aspirin boast.

Researchers tested 11 young men, who were asked to undergo "exhaustive aerobic exercises" by riding stationary bikes till they reached the point of exhaustion.

After the completion of the sessions, each subject was given a Swedish-style massage on one of their legs.

The other received no such treatment and was treated as point of comparison. The test subjects then underwent gene-profiling techniques in order to check the chemical changes in their muscle cells.

The first impact was that it switched on the genes involved in inflammation reduction. In addition, it activated the genes that promote the creation of mitochondria - structures that are the energy factories inside cells. The fitter a muscle cell is the more mitochondria it tends to have.

Telomere Nobelist: Selling a 'biological age' DNA test for ageing

Elizabeth Blackburn is launching a commercial genetic test that measures DNA markers of ageing – what can we learn from it?

Your test measures telomere shortening, a marker of biological ageing. What can this tell us?
Telomeres are stretches of DNA at the ends of chromosomes that protect them against degradation. 

Checking your telomere length is a bit like weighing yourself: you get this single number which depends on a lot of factors. Telomere length gives a sense of your underlying health. We see telomere shortening in diseases of ageing - like heart disease and cancer.

What evidence is there to support health predictions based on telomere length?
In 2004, results from a study that I worked on with colleagues at the University of California, San Francisco, linked chronic stress to shortening of telomeres. 

Chronic stress is also associated with a higher risk of heart disease. Bone marrow failure is also associated with short telomeres. If a test showed you had telomere shortening, it would be a red flag suggesting you should take a look at possible risk factors.

Can people do anything to prevent telomere shortening?
It looks like you can, by changing your lifestyle. Observational studies show that exercise, nutritional supplements and reducing psychological stress can help. Chronic high stress and smoking can lead to accelerated telomere shortening.

What made you decide to help launch the company Telome Health, which is selling a test for telomere length?
There was a lot of interest from the research community and also from individuals. We had a cost-effective assay in our lab which we transferred to a company to provide as a service. We are running a study called "Know your telomeres". 

The goal is to learn more about telomere length and other markers of ageing, how best to measure these markers, how they are related to health and lifestyle, and how people respond to learning their own telomere length results. People were pounding down the doors to enrol.

Is this another step on the road to commercialised personal genetic testing?
Right now, the company only offers the tests as a part of research studies. Tests for the public, through their physician, will go on sale later in the year, costing under $200.

What exactly does the telomere test entail?
It is like a cholesterol test. We can take a measurement from blood samples, cheek swabs or saliva. Specifically, we measure the telomere length in white blood cells. Cells from the immune system act a bit like a report card, an indicator for all kinds of conditions.

Have you made any lifestyle changes based on the results of your research?
I've learned a meditation technique. I exercise as often as I can. Walking is good too.

Malaria: Turning the Genetic Keys to switch it off

More than a third of the 72 molecular switches that control key stages in the life cycle of the malaria parasite can be disrupted in some way.

The finding is a significant breakthrough in the search for inexpensive, effective vaccines and drugs to stop the transmission of a disease that kills up to a million children a year, according to new research.

Until now little has been known about the cellular processes involved in the development of this deadly disease.

The research, published in the journal Cell Host & Microbe, involved the first comprehensive functional analysis of protein kinases in any malaria parasite.

It is also the largest gene knock-out study in Plasmodium berghei—a malaria parasite infecting rodents.

“Blocking parasite transmission is recognized as an important element in the global fight to control malaria,” says Rita Tewari, in the school of biology at the University of Nottingham.

“Kinases are a family of proteins which contribute to the control of nearly all cellular processes and have already become major drug targets in the fight against cancer and other diseases.

“Now we have identified some key regulators that control the
transmission of the malaria parasite. Work to develop drugs to eradicate this terrible disease can now focus on the best targets.

This study shows how systematic functional studies not only increase our knowledge in understanding complexity of malaria parasite development but also gives us the rational approach towards drug development.”

More.....

University of Nottingham: http://communications.nottingham.ac.uk/News.html

Gene switch rejuvenates failing mouse brains

Gene switch rejuvenates failing mouse brains

Step aside, Sudoku. A genetic switch that causes memory impairment in ageing mice when it goes into "off" mode has been flicked on, restoring failing brains to a more youthful state.

If a similar switch can be found in people, it might provide a new way to keep ageing human brains young.
Cognitive decline, particularly memory impairment, is a normal part of ageing in humans and animals. Yet why this happens, and how we can prevent it, is largely unknown, says David Sweatt at the University of Alabama, Birmingham, who was not involved in the new work.

André Fischer of the European Neuroscience Institute in Göttingen, Germany, and colleagues forced 3-month-old mice to find their way around a new environment and assessed them on their ability to associate an electric shock with a particular environment.

New neurons
The result was increased activity of a cluster of over 1500 genes which are known make proteins that are needed for the creation of new neurons – a process that is necessary for learning in humans and mice.

This boost in gene expression did not occur in 16-month-old mice given the same tasks: the activity of their genes changed only slightly. The mice also did worse than the young ones at spatial learning and memory tasks.

To uncover what prevents elderly mice getting this genetic boost, Fischer analysed the DNA found in neurons in the hippocampus of both old and young mice.

They found that when young mice are learning, a molecular fragment known as an acetyl group binds to a particular point on the histone protein that DNA wraps itself around – with the result that the cluster of learning and memory genes on the surrounding DNA ends up close to the acetyl group.

DNA 'on' switch
This acetyl "cap" was missing in the older mice that had been set the same tasks. From this, the team concludes that the cap acts as an "on" switch for the cluster of learning and memory genes: removing the cap switches off the genes.

Next, by injecting an enzyme known to encourage caps to bind to any kind of histone molecule, Fischer's team artificially flipped the switch to the on position in old mice. The acetyl group returned to the histone molecule and the mice's learning and memory performance became similar to that of 3-month-old mice.