Scientists have discovered a microbe that stays young forever by rejuvenating every time it reproduces, a finding that provides fundamental insights into the mechanisms of ageing.

An international team involving researchers from the University of Bristol and the Max-Planck Institute for Molecular Cell Biology and Genetics in Germany has found that a common species of yeast microbe has evolved to stay young.

The organism could potentially serve as a model of certain non-ageing types of cells in humans, researchers said.

The team has shown that, unlike other species, the yeast microbe called S pombe, is immune to ageing when it is reproducing and under favourable growth conditions.

In general, even symmetrically diving microbes, do not split into two exactly identical halves.

Detailed investigations revealed that there are mechanisms in place that ensure that one half gets older, often defective, cell material, whereas the other half is equipped with new fully-functional material.

So like humans microbes, in a sense, produce offspring that is younger than the parent.

However, ageing is not inevitable for the common yeast, S pombe. Researchers found that this microbe is immune to ageing under certain conditions.

When the yeast is treated well, it reproduces by splitting into two halves that both inherit their fair share of old cell material.

"However, as both cells get only half of the damaged material, they are both younger than before," said Iva Tolic, the lead investigator on the project.

At least in a sense, the yeast is rejuvenated a bit, every time it reproduces, Tolic said.

Unlike other species S pombe can escape ageing as long as it keeps dividing fast enough.

To test what happens to the microbe when it is treated badly, the researchers exposed the yeast to heat, ultraviolet radiation, and damaging chemicals, which slowed its growth to a point where the microbes could not divide fast enough to stay young.

Once subjected to these negative influences the yeast cells started splitting into a younger and an older half just like other cells. While the older cells eventually died, their offspring survived long enough to reproduce even in the harsh environments.

The findings are published in the journal Current Biology.

An Indian scientist has claimed that evidence from people suffering from heart disease supports the existence of the molecular link first discovered in laboratory mice between the body's natural circadian rhythms and cardiac arrest or sudden cardiac death.

Mukesh Jain, M.D., said that it pinpoints a previously unrecognized factor in the electrical storm that makes the heart's main pumping chambers suddenly begin to beat erratically in a way that stops the flow of blood to the brain and body.

Termed ventricular fibrillation, the condition causes sudden cardiac death (SCD), in which the victim instantly becomes unconscious and dies unless CPR or a defibrillator is available to shock the heart back into its steady beat.

The peak risk hours when SCD strikes range from 6 am to 10 am, with a smaller peak in the late afternoon. Scientists long suspected a link between SCD and the 24-hour body clock, located in the brain.

It governs 24-hour cycles of sleep and wakefulness called circadian rhythms that coordinate a range of body functions with the outside environment.

Jain's group discovered a protein called KLF15 that helps regulate the heart's electrical activity, and occurs in the body in levels that change like clockwork throughout the day. KLF15 helps form channels that allow substances to enter and exit heart cells in ways critical to maintaining a normal, steady heartbeat.

They first discovered that patients with heart failure have lower levels of KLF15. Then, they established in laboratory mice that KLF15 is the molecular link between SCD and the circadian rhythm. And mice with low levels of the protein have the same heart problems as people with SCD.

A physician has said that the reason behind the slow progress in researchers` quest for the cause of multiple sclerosis is that most of the research has targeted the wrong part of the brain.

Steven Schutzer, a physician and scientist at Rutgers New Jersey Medical School, attacked the problem from a different direction. He is one of the first scientists to analyze patients` cerebrospinal fluid (CSF) by taking full advantage of a combination of technologies called proteomics and high-resolution mass spectrometry.

He said that proteins present in the clear liquid that bathes the central nervous system can be a window to physical changes that accompany neurological disease and the latest mass spectrometry techniques allow us to see them as never before.

In this study, Schutzer used that novel approach to compare the cerebrospinal fluid of newly diagnosed MS patients with that of longer term patients, as well as fluid taken from people with no signs of neurological disease.

What Schutzer found startled one of his co-investigators, Patricia K. Coyle of Stony Brook University in New York, one of the leading MS clinicians and researchers in the country.

The proteins in the CSF of the new MS patients suggested physiological disruptions not only in the white matter of the brain where the myelin damage eventually shows up.

They also pointed to substantial disruptions in the gray matter, a different part of the brain that contains the axons and dendrites and synapses that transfer signals between nerves.

The new findings have been published in the journal PLOS ONE.

Researchers have suggested that the cell transplants could be used to treat schizophrenia.

Senior author Daniel Lodge, Ph.D., assistant professor of pharmacology in the School of Medicine at the University of Texas Health Science Center at San Antonio, said that since these cells are not functioning properly, our idea is to replace them.

Lodge and lead author Stephanie Perez, graduate student in his laboratory, biopsied tissue from rat fetuses, isolated cells from the tissue and injected the cells into a brain center called the hippocampus.

This center regulates the dopamine system and plays a role in learning, memory and executive functions such as decision making. Rats treated with the transplanted cells have restored hippocampal and dopamine function.

Lodge said that they put in a lot of cells and not all survived, but a significant portion did and restored hippocampal and dopamine function back to normal.

The study has been published in Molecular Psychiatry.

Scientists have uncovered a genetic link specific to the risk of childhood leukaemia.

Study author Kenneth Offit, MD, MPH, Chief of the Clinical Genetics Service at Memorial Sloan-Kettering Cancer Center, said that at the very least the discovery gives us a new window into inherited causes of childhood leukemia.

Offit said that more immediately, testing for this mutation may allow affected families to prevent leukemia in future generations.

The mutation was first observed in a family treated at Memorial Sloan-Kettering of which several family members of different generations had been diagnosed with childhood acute lymphoblastic leukemia (ALL).

A second, non-related, leukemia-prone family cared for at a different hospital was later found to have the same mutation. A series of experiments were conducted confirming that the observed mutation compromised the normal function of the gene, which may increase the risk of developing ALL.

The inherited genetic mutation is located in a gene called PAX5, which is known to play a role in the development of some B cell cancers, including ALL.

The findings have been published in the journal Nature Genetics.