Working at the University of Oxford and The Open University, Dr Lynne Cox and Dr Robert Saunders say they have found a fast and effective way to investigate important aspects of human aging.

Their discovery of a gene in fruit flies means they can now be used to study the effects aging has on DNA. The researchers demonstrate the value of this model in helping us to understand the critical aspects of human aging at cellular, genetic and biochemical levels.

Dr Lynne Cox from the University of Oxford said: "We study a premature human ageing disease called Werner syndrome to help us understand normal aging. The key to this disease is that changes in a single gene (called WRN) mean that patients age very quickly. Scientists have made great progress in working out what this gene does in the test tube, but until now we haven’t been able to investigate the gene to look at its effect on development and the whole body. By working on this gene in fruit flies, we can model human aging in a powerful experimental system."

At first, fruit flies eat like horses. Hatching inside over-ripe fruit where they were laid, they feed wildly in the sugar-rich environment until nature sends them an offer they can’t refuse. To survive, they must leave the fruit, wander off and burrow into the earth where they avoid food as if it were poison. Only then can the larvae grow and hatch into flies that will take wing to lay their own eggs.

Now, a team of researchers from the University of Georgia has discovered for the first time that the important developmental switch from food attraction to aversion in the fruit fly larva is controlled by a timing mechanism in the brain and its sensory system. The study shows how this important avoidance mechanism has been recruited into evolutionary processes to promote development and could one day lead to new methods of controlling pain in humans and other animals.

Fruit flies can’t really stay in the rotting fruit where they are laid. Not only do they risk drowning in the ripening fluid, they are increasingly exposed to harmful microorganisms that can kill them. To escape, the larvae “wander” out and burrow into the ground.

A protein that is indispensable for passing on an accurate copy of the genome from mother to daughter cells can be compared to a cowboy’s lasso, say scientists at the The FIRC Institute of Molecular Oncology Foundation (IFOM).

It 'catches' chromosomes and ties them to a transitory structure assembled during cell division. Once they have been neatly tied up, the chromosomes await the end of replication to be equally distributed between the two daughter cells. But if the lasso doesn’t catch them, chromosomes end up being randomly scattered, with potentially disastrous genetic effects: should cells survive this, they receive the wrong genetic inheritance, with dire consequences.

This study opens up new avenues of research to reduce the toxicity of chemotherapy in the treatment of cancer.

A new study by UC Davis researchers provides evidence that methods using human bone marrow-derived stem cells to deliver gene therapy to cure diseases of the blood, bone marrow and certain types of cancer do not cause the development of tumors or leukemia. The study was published online in the May 6, 2008 issue of Molecular Therapy.

"The results of our decade-long study of adult human stem cell transplantation shows that there is little risk of adverse events caused by gene transfer, and that adult human stem cells do not pose a cancer risk when implanted into different organs," said Jan Nolta, senior author of the study and director of the UC Davis Stem Cell Program.

Nolta and her colleagues tested the safety of gene transfer into bone marrow stem cells from human donors in more than 600 mice. None of the transplanted mice developed leukemia or solid tumors caused by the gene therapy treatment, during the evaluation period of up to 18 months.

Imagine being able to tone down appetite and promote weight loss, while improving the body’s ability to handle blood sugar levels.

That’s just what Tony Means, PhD, and his team at the Duke University Medical Center were able to do when they blocked a brain enzyme, CaMKK2, in mice.

“We believe we have identified an important drug development target that could potentially turn into a metabolic triple play: appetite control, weight loss and blood sugar management,“ said Means, who is the Nanaline H. Duke Professor and Chairman of Pharmacology and Cancer Biology.

A process of self-digestion called autophagy prompts the maturation of red blood cells. Without a protein called Nix, the cells would not effectively rid themselves of organelles called mitochondria and consequently become short-lived, leading to anemia, said researchers at Baylor College of Medicine in Houston.

“It’s changed our thinking on autophagy,” said Dr. Jin Wang, assistant professor of immunology at BCM and senior author of the report in Nature. During autophagy, the cell forms an envelope or vesicle around components of the cell that need to be degraded and removed. The vesicle then fuses with a cellular component called a lysosome that degrades its contents. The inclusion of components in the cell by autophagy vesicles was generally considered to be nonspecific.

'Clone' is an odd term culturally. Thanks to science fiction on one side and ethical hysteria on the other, people tend to overstate the meaning of it.

Back before genomes, to 'clone a gene' was to basically discover it - it meant you found the stretch of DNA encoding that gene - but now we know where almost all of the genes are. So 'cloning' in this context does not mean 'discovery' and it certainly doesn't mean Sith Lords spitting out an army of warriors to take over the universe - it means taking known genes (in tiny pieces in the genome) and isolating the spliced versions into a format that can be used in the lab.

While a few human genomes have been sequenced, the real work of understanding cancer (and curing it) is still a long way off because most human genes have not been isolated.

Metastasis, the spread of cancer throughout the body, can be explained by the fusion of a cancer cell with a white blood cell in the original tumor, according to Yale School of Medicine researchers, who say that this single event can set the stage for cancer’s migration to other parts of the body.

The studies, spanning 15 years, have revealed that the newly formed hybrid of the cancer cell and white blood cell adapts the white blood cell’s natural ability to migrate around the body, while going through the uncontrolled cell division of the original cancer cell. This causes a metastatic cell to emerge, which like a white blood cell, can migrate through tissue, enter the circulatory system and travel to other organs.

Maturity, in some respects, brings diminished possibilities. As a fertilized egg cell repeatedly divides to grow into a mature animal, most of the resulting cells become ever more specialized.

But a small number of cells, known as stem cells, remain uncommitted even as they spawn more specialized progeny. The most versatile stem cells, taken from days-old embryos, are able to form any cell type — but studying them in people is controversial.

Even in adults, however, other types of stem cells persist that have a more limited repertoire. Some replace specific cells as they wear out; others help to rebuild damaged tissues. Still other stem cells are suspected by some scientists of starting or maintaining cancers.

Now team of researchers led by scientists at Cold Spring Harbor Laboratory have for the first time identified stem cells that allow the pituitary glands of mice to grow even after birth.

New heart research published inNature Genetics reveals how a gene called osteoglycin (Ogn), which had not previously been linked with heart function, plays a key role in regulating heart growth. The study suggests that the gene can behave abnormally in some people, and that this can lead to the heart becoming abnormally enlarged.

The researchers hope that through understanding how enlarged hearts are linked to the workings of genes like Ogn, they will be able to develop new treatments for the condition, which affects a large proportion of those with high blood pressure, obesity and diabetes.

Scientists believe that enlarged hearts are caused by a combination of genetic factors and external stimuli such as high blood pressure and obesity. However, the role played by genes has remained largely unknown.