Tuesday, October 6, 2009

WELCOME to More FACT than FICTION by K.E.Perrott author of 'INFINITY 48'

Welcome.

The 2009 Nobel Prize in Physiology or Medicine has been awarded to 3 Marvellous Human Beings. An Australian - Elizabeth.H.Blackburn, an American - Carol.W.Greider and Jack.W.Szostak from England. Awarded for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase.
I've written about chromosomes, stem cells and telemeres being the bases for eternal youth and good health for humans in my novel 'Infinity 48'. It's exciting stuff!
My novel is based upon real science and expanded on to show readers real possibilities for future humans. Some of the ideas in 'Infinity 48' could be a reality sooner than later.
The following article is about real scientists and their incredible hard work and earth-shattering breakthroughs. I've included the article from the nobelprize.org website for your convenience, it's well worth a read. You might also like to visit the website for more great articles.

Nobel Prize® medal - registered trademark of the Nobel Foundation

The Nobel Prize in Physiology or Medicine 2009

Nobel Assembly logo

Press Release

5 October 2009

The Nobel Assembly at Karolinska Institutet has today decided to award
The Nobel Prize in Physiology or Medicine 2009 jointly to

Elizabeth H. Blackburn, Carol W. Greider and Jack W. Szostak

for the discovery of

"how chromosomes are protected by telomeres and the enzyme telomerase"

Summary

This year's Nobel Prize in Physiology or Medicine is awarded to three scientists who have solved a major problem in biology: how the chromosomes can be copied in a complete way during cell divisions and how they are protected against degradation. The Nobel Laureates have shown that the solution is to be found in the ends of the chromosomes – the telomeres – and in an enzyme that forms them – telomerase.

The long, thread-like DNA molecules that carry our genes are packed into chromosomes, the telomeres being the caps on their ends. Elizabeth Blackburn and Jack Szostak discovered that a unique DNA sequence in the telomeres protects the chromosomes from degradation. Carol Greider and Elizabeth Blackburn identified telomerase, the enzyme that makes telomere DNA. These discoveries explained how the ends of the chromosomes are protected by the telomeres and that they are built by telomerase.

If the telomeres are shortened, cells age. Conversely, if telomerase activity is high, telomere length is maintained, and cellular senescence is delayed. This is the case in cancer cells, which can be considered to have eternal life. Certain inherited diseases, in contrast, are characterized by a defective telomerase, resulting in damaged cells. The award of the Nobel Prize recognizes the discovery of a fundamental mechanism in the cell, a discovery that has stimulated the development of new therapeutic strategies.

The mysterious telomere

The chromosomes contain our genome in their DNA molecules. As early as the 1930s, Hermann Muller (Nobel Prize 1946) and Barbara McClintock (Nobel Prize 1983) had observed that the structures at the ends of the chromosomes, the so-called telomeres, seemed to prevent the chromosomes from attaching to each other. They suspected that the telomeres could have a protective role, but how they operate remained an enigma.

When scientists began to understand how genes are copied, in the 1950s, another problem presented itself. When a cell is about to divide, the DNA molecules, which contain the four bases that form the genetic code, are copied, base by base, by DNA polymerase enzymes. However, for one of the two DNA strands, a problem exists in that the very end of the strand cannot be copied. Therefore, the chromosomes should be shortened every time a cell divides – but in fact that is not usually the case (Fig 1).

Both these problems were solved when this year's Nobel Laureates discovered how the telomere functions and found the enzyme that copies it.

Telomere DNA protects the chromosomes

In the early phase of her research career, Elizabeth Blackburn mapped DNA sequences. When studying the chromosomes of Tetrahymena, a unicellular ciliate organism, she identified a DNA sequence that was repeated several times at the ends of the chromosomes. The function of this sequence, CCCCAA, was unclear. At the same time, Jack Szostak had made the observation that a linear DNA molecule, a type of minichromosome, is rapidly degraded when introduced into yeast cells.

Blackburn presented her results at a conference in 1980. They caught Jack Szostak's interest and he and Blackburn decided to perform an experiment that would cross the boundaries between very distant species (Fig 2). From the DNA of Tetrahymena, Blackburn isolated the CCCCAA sequence. Szostak coupled it to the minichromosomes and put them back into yeast cells. The results, which were published in 1982, were striking – the telomere DNA sequence protected the minichromosomes from degradation. As telomere DNA from one organism, Tetrahymena, protected chromosomes in an entirely different one, yeast, this demonstrated the existence of a previously unrecognized fundamental mechanism. Later on, it became evident that telomere DNA with its characteristic sequence is present in most plants and animals, from amoeba to man.

An enzyme that builds telomeres

Carol Greider, then a graduate student, and her supervisor Blackburn started to investigate if the formation of telomere DNA could be due to an unknown enzyme. On Christmas Day, 1984, Greider discovered signs of enzymatic activity in a cell extract. Greider and Blackburn named the enzyme telomerase, purified it, and showed that it consists of RNA as well as protein (Fig 3). The RNA component turned out to contain the CCCCAA sequence. It serves as the template when the telomere is built, while the protein component is required for the construction work, i.e. the enzymatic activity. Telomerase extends telomere DNA, providing a platform that enables DNA polymerases to copy the entire length of the chromosome without missing the very end portion.

Telomeres delay ageing of the cell

Scientists now began to investigate what roles the telomere might play in the cell. Szostak's group identified yeast cells with mutations that led to a gradual shortening of the telomeres. Such cells grew poorly and eventually stopped dividing. Blackburn and her co-workers made mutations in the RNA of the telomerase and observed similar effects in Tetrahymena. In both cases, this led to premature cellular ageing – senescence. In contrast, functional telomeres instead prevent chromosomal damage and delay cellular senescence. Later on, Greider's group showed that the senescence of human cells is also delayed by telomerase. Research in this area has been intense and it is now known that the DNA sequence in the telomere attracts proteins that form a protective cap around the fragile ends of the DNA strands.

An important piece in the puzzle – human ageing, cancer, and stem cells

These discoveries had a major impact within the scientific community. Many scientists speculated that telomere shortening could be the reason for ageing, not only in the individual cells but also in the organism as a whole. But the ageing process has turned out to be complex and it is now thought to depend on several different factors, the telomere being one of them. Research in this area remains intense.

Most normal cells do not divide frequently, therefore their chromosomes are not at risk of shortening and they do not require high telomerase activity. In contrast, cancer cells have the ability to divide infinitely and yet preserve their telomeres. How do they escape cellular senescence? One explanation became apparent with the finding that cancer cells often have increased telomerase activity. It was therefore proposed that cancer might be treated by eradicating telomerase. Several studies are underway in this area, including clinical trials evaluating vaccines directed against cells with elevated telomerase activity.

Some inherited diseases are now known to be caused by telomerase defects, including certain forms of congenital aplastic anemia, in which insufficient cell divisions in the stem cells of the bone marrow lead to severe anemia. Certain inherited diseases of the skin and the lungs are also caused by telomerase defects.

In conclusion, the discoveries by Blackburn, Greider and Szostak have added a new dimension to our understanding of the cell, shed light on disease mechanisms, and stimulated the development of potential new therapies.

Elizabeth H. Blackburn has US and Australian citizenship. She was born in 1948 in Hobart, Tasmania, Australia. After undergraduate studies at the University of Melbourne, she received her PhD in 1975 from the University of Cambridge, England, and was a postdoctoral researcher at Yale University, New Haven, USA. She was on the faculty at the University of California, Berkeley, and since 1990 has been professor of biology and physiology at the University of California, San Francisco.

Carol W. Greider is a US citizen and was born in 1961 in San Diego, California, USA. She studied at the University of California in Santa Barbara and in Berkeley, where she obtained her PhD in 1987 with Blackburn as her supervisor. After postdoctoral research at Cold Spring Harbor Laboratory, she was appointed professor in the department of molecular biology and genetics at Johns Hopkins University School of Medicine in Baltimore in 1997.

Jack W. Szostak is a US citizen. He was born in 1952 in London, UK and grew up in Canada. He studied at McGill University in Montreal and at Cornell University in Ithaca, New York, where he received his PhD in 1977. He has been at Harvard Medical School since 1979 and is currently professor of genetics at Massachusetts General Hospital in Boston. He is also affiliated with the Howard Hughes Medical Institute.

References:
Szostak JW, Blackburn EH. Cloning yeast telomeres on linear plasmid vectors. Cell 1982; 29:245-255.
Greider CW, Blackburn EH. Identification of a specific telomere terminal transferase activity in Tetrahymena extracts. Cell 1985; 43:405-13.
Greider CW, Blackburn EH. A telomeric sequence in the RNA of Tetrahymena telomerase required for telomere repeat synthesis. Nature 1989; 337:331-7.

The Nobel Assembly, consisting of 50 professors at Karolinska Institutet, awards the Nobel Prize in Physiology or Medicine. Its Nobel Committee evaluates the nominations. Since 1901 the Nobel Prize has been awarded to scientists who have made the most important discoveries for the benefit of mankind.

Nobel Prize® is the registered trademark of the Nobel Foundation

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To read pages or purchase your copy of 'Infinity 48' at a great discount, please visit: www.infinity48.com

To visit the Nobel Prize site please visit: www.nobelprize.org

Bye for now, and good thinking.

Monday, October 5, 2009

'Infinity 48' by K.E.Perrott. Explosive new thinking!

WELCOME to More Fact than Fiction, by K.E.Perrott. Here I hope you find yourself thinking outside the box, questioning everything and comfortable with that.

This is a great article, in case you missed it I've included it here for you.


Fossil finds extend human story
By Jonathan Amos
Science reporter, BBC News

An ancient human-like creature that may be a direct ancestor to our species has been described by researchers.

The assessment of the 4.4-million-year-old animal called Ardipithecus ramidus is reported in the journal Science.

Even if it is not on the direct line to us, it offers new insights into how we evolved from the common ancestor we share with chimps, the team says.

Fossils of A. ramidus were first found in Ethiopia in 1992, but it has taken 17 years to assess their significance.

The most important specimen is a partial skeleton of a female nicknamed "Ardi".

If Ardipithecus ramidus was not actually the species directly ancestral to us, she must have been closely related to it
The Ardipithecus project team

The international team has recovered key bones, including the skull with teeth, arms, hands, pelvis, legs, and feet.

But the researchers have other fragments that may represent perhaps at least 36 different individuals, including youngsters, males, and females.

One of the lead scientists on the project, Professor Tim White from the University of California, Berkeley, said the investigation had been painstaking.

"It took us many, many years to clean the bones in the National Museum of Ethiopia and then set about to restore this skeleton to its original dimensions and form; and then study it and compare it with all the other fossils that are known from Africa and elsewhere, as well as with the modern age," he told the journal.

"This is not an ordinary fossil. It's not a chimp. It's not a human. It shows us what we used to be."

Tree life

The fossils come from the Middle Awash study area in the Afar Rift, about 230km northeast of Addis Ababa, Ethiopia's capital.

Some of the characteristics of the animal's skeleton are said to echo features seen in very ancient apes; others presage traits seen in later, more human-like species.

The scientists say 1.2m-high (4ft) Ardi was good at climbing trees but also walked on two feet. However she did not have arched feet like us, indicating that she could not walk or run for long distances.

"She has opposable great toes and she has a pelvis that allows her to negotiate tree branches rather well," explained team-member Professor Owen Lovejoy, from Kent State University, Ohio.

"So half of her life is spent in the trees; she would have nested in trees and occasionally fed in trees, but when she was on the ground she walked upright pretty close to how you and I walk," he told BBC News.

That she lived in what would have been a wooded area 4.4 million years ago is somewhat challenging, says the team. It had been thought that early human evolution was driven, if only in part, by the disappearance of trees - encouraging our ancestors to walk on the ground.

"These creatures were living and dying in a woodland habitat, not an open savannah," said Professor White.

Because of its age, Ardipithecus is said to take science closer to the yet-to-be-found last common ancestor with chimps, our close genetic relatives.

And because many of Ardipithecus ' traits do not appear in modern-day African apes, it suggests this common ancestor may have existed much further back in time than had previously been supposed - perhaps seven or nine million years ago.

Comparisons with modern chimp and gorilla anatomy also underline just how much these African apes themselves have evolved since parting company with the line that led eventually to modern humans.

Rapid evolution

Asked whether A. ramidus was our direct ancestor or not, the team said more fossils from different places and time periods were needed to answer the question.

"We will need many more fossil recoveries from the period of 3-5 million years ago to confidently answer that question in the future," the scientists said in a briefing document that accompanied their journal papers.

"But if Ardipithecus ramidus was not actually the species directly ancestral to us, she must have been closely related to it, and would have been similar in appearance and adaptation.

Independent experts in the field are struck by how primitive Ardipithecus appears compared with the Australopithecines, another group of hominid (human-like) creatures from Africa that lived slightly nearer to us in time.

One species in particular, Australopithecus afarensis , the famous "Lucy" fossil found in 1974, is very strongly linked into the human story because of its developed walking ability.

For Ardipithecus ramidus to also sit on that direct line seemed to require some rapid evolutionary change, commented Professor Chris Stringer from London's Natural History museum.

"With Australopithecus starting from four million years ago, one would have thought that things would have moved further down the line by 4.4 million years ago," he told BBC News.

"OK, you can have very rapid change, perhaps; or Ardipithecus might be a residual form, a relic of a somewhat older stage of evolution that had carried on. Perhaps we will find something more like Australopithecus at 4.4 million years old somewhere else in Africa."

Jonathan.Amos-INTERNET@bbc.co.uk




To purchase your copy of 'Infinity 48' at a great discount please visit: www.infinity48.com
Bye for now, and good thinking!