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This press release is copyright Nature. VOL.440 NO.7087 DATED 20 April 2006
This press release contains:
* Summaries of newsworthy papers:
- Social evolution: how exactly did we all start cooperating?
- Commentary: Learning from Chernobyl
- Cell biology: Regular recycling saves lives
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[6] Social evolution: how exactly did we all start cooperating? (pp1045-1049)
Human societies are notable for the prevalence of cooperation, but the origins of this behaviour are confusing, especially given the potential benefits for anyone prepared to take advantage of others' kindness. Traditionally, this has been investigated using simple 'game theory' tests in which people or computers are given a simple choice of different strategies, such as cheating or helping a fellow player. But these models lack the sophistication of the real world.
A new, more sophisticated computer model now shows that a range of cooperative strategies can arise spontaneously, as long as people are free to see whether others are similarly imbued with community spirit. Agents in the computer model occupy a matrix of virtual squares, and can 'choose' either to rest, eat, reproduce or attack a neighbour.
A range of different strategies emerges, say the model's developers Mikhail Burtsev and Peter Turchin in this week's Nature. Alongside the aggressive 'hawks' and docile 'doves' seen in previous game-theory exercises, other options arise, such as 'ravens', which fight with others but get along fine with their own kind, and 'starlings', which clump together and share resources in the knowledge that their strength of numbers allows them to repel invaders.
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Mikhail Burtsev (Keldysh Institute of Applied Mathematics of RAS, Moscow, Russia)
Tel: +7 903 561 4149; E-mail: [email protected]
Commentary: Learning from Chernobyl (pp933-934) (pp982-983)
As the 20-year anniversary of Chernobyl approaches, a Commentary and Special News Report in Nature this week investigate the health effects of radioactive fallout, particularly in the light of a United Nations (UN) report assessing the effects of the disaster.
Last year's prediction by the UN Chernobyl Forum of a maximum of 9,000 radiation-related deaths in regions heavily contaminated by Chernobyl is too reassuring, given the massive uncertainties, argue Dillwyn Williams and Keith Baverstock. The lesson of the atomic bombs in Nagasaki and Hiroshima is that 20 years is too soon to be able to predict all the consequences of fallout.
Although the type of radiation exposure was different in Japan, the Radiation Effects Research Foundation set up to study the bombs' legacy should be a model for coordinated monitoring of possible health consequences, they argue. At the very least, say the authors, there should be comprehensive studies on the hundreds of thousands of people in the most affected areas of Belarus, Ukraine and Russia. Williams and Baverstock believe that unless a full and independent study of the consequences of Chernobyl is established, public mistrust of the nuclear industry will continue.
In a Special News Report on the same topic, Mark Peplow further explores the arguments over the disaster's death toll. Scientists cited in the UN report are concerned about how their figures are presented. They argue that the true cost of the disaster will not be known for decades, if ever. The report investigates how these figures were reached, and what further monitoring should be done before further predictions can be made.
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Dillwyn Williams (Strangeways Research Laboratories, Cambridge, UK)
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[7] & [8] Cell biology: Regular recycling saves lives (AOP)
DOI: 10.1038/nature04723
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***These papers will be published electronically on Nature's website on 19 April at 1800 London time / 1300 US Eastern time (which is also when the embargo lifts) as part of our AOP (ahead of print) programme. Although we have included them on this release to avoid multiple mailings they will not appear in print on 20 April, but at a later date.***
The process of protein degradation and clearance of cellular components may be more important in maintaining the nervous system and keeping neurodegeneration at bay than was previously understood, according to two papers to be published online by Nature this week.
Autophagy - protein degradation and recycling of cellular components - is important for the normal growth and development of a cell. Two research teams now show that inhibiting this process in mouse brain cells results in neurodegeneration and early death.
In the first paper, Keiji Tanaka and colleagues create mice with a neural-cell-specific deficiency in the Atg7 gene, which encodes a key enzyme essential for autophagosome formation. These mice exhibited a reduction in coordinated movement, and a massive buildup of proteins and loss of neurons in the cerebral and cerebellar cortices, which led to a premature death 28 weeks after birth. In the second paper, Noboru Mizushima and colleagues knocked out the Atg5 gene. These mice also developed progressive motor-function impairment and tremors, which were accompanied by the accumulation of cytoplasmic protein-containing inclusion bodies in neurons. Both papers show that the continual clearance of cellular components is essential for maintaining neuronal health and opens new avenues of research to tackle neurodegenerative disease.
CONTACT
Keiji Tanaka (The Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan)
Tel: +81 3 3823 2237; E-mail: [email protected] Paper [7]
Noboru Mizushima (The Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan)
Tel: +81 3 4463 7590; E-mail: [email protected] Paper [8]
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