Also consider that same railgun system as a possible defense for asteroids, meteors, and comets that might be on an impact trajectory with Earth in the future. This could be a major reason for having a military base on the moon. As it stands currently, we have no line of defense for such impacts.
And then there is the other big science fiction possibility-mathematically it is a finite probability-that the Earth is invaded by aliens. Having our military in multiple locations might be useful in that situation. Having humanity spread out in multiple places wouldn’t be a bad idea, either.
Well, one thing for certain though, militarization of the moon is a long way off. So, if you are one of those types that is opposed to such an idea, then don’t panic. There is plenty of civilian exploration to be had on the moon. There is plenty of science to discover and uncover on the moon. Perhaps some smart entrepreneur will develop an economically viable business model for moon missions. Maybe there will be a Club Med Tranquility Base in the not so distant future.
Whatever the outcome is, the thing to remember is that there is a big bright future for space exploration that starts on the moon. And, if there are ideas that you have for reasons for going and staying on the moon, by all means don’t keep them to yourself. NASA is looking for great ideas and applications for space travel. What to do once we get to the moon is such a question that Administrator Griffin had these words to pass along in an E-mail to his upper echelon advisors:
The next step out is the moon. We're going to get, and probably already are getting, the same criticisms as for ISS. This is the "why go to the moon?" theme.
We've got the architecture in place and generally accepted. That's the "interstate highway" analogy I've made. So now, we need to start talking about those exit ramps I've referred to. What ARE we going to do on the moon? To what end? And with whom? I have ideas, of course. (I ALWAYS have ideas; it's a given.) But my ideas don't matter. Now is the time to start working with our own science community and with the Internationals to define the program of lunar activity that makes the most sense to the most people. I keep saying-because it's true-that it's not the trip that matters, it's the destination, and what we do there. We’ve got to get started on this.
… and the International Partners to get started down the track on pulling together an international coalition. They are annoyed and impatient with our delays since the Vision speech. We need to be, and be seen to be, proactive in seeking their involvement. We need to work with them, not prescribe to them, regarding what we can do together on the moon.
Beyond the moon is Mars, robots first. Most of the Internationals are at present more interested in Mars, as I hear the gossip. Fine, we can't tell them what to be interested in. But our road to Mars goes through the moon, and we should be able to enlist them to join on that path.
Everyone… wants to be part of making exploration what NASA does. It won't survive if all we worry about is getting there. That was the essential first step. But it has to sell itself on what it is that we DO there.
So When are We Going?
As the program currently stands, NASA plans to be testing the systems for the CEV as early as this year. Design studies and reviews are to begin no later than 2008. Suborbital flight testing of the spacecraft is to begin sometime around 2009 to 2010. There are at least three so-called “risk reduction flights” scheduled between 2010 and 2012. The hopes are to have the CEV flights proven and ready for operation by 2012. This will allow decommissioning of the shuttles as the CEV will be able to transport crewmembers to the ISS.
The heavy launch vehicle, CLV, will be developed parallel to the CEV. However, the flight readiness of the CEV seems to have priority status. The current NASA plan is to implement what Griffin refers to as the “Lunar Sooner” plan that will see flight testing of the CLV sometime between 2013 to 2016 with flight readiness soon after. The “Lunar Sooner” plan optimistically has the CEV and CLV ready for the first manned Moon mission by March of 2017! That is only eleven years away and is three years ahead of the original schedule suggested by President Bush. So just be patient, we are liable to make it back to the moon within the lifetimes of the majority of people that are reading this article!
ADD NOTE:
"Since this article was written NASA has solidified the CEV program more and has chosen new descriptions for the launch vehicle systems. The small capsule that carries the crew will be the Crew Exploration Vehicle or CEV. The modified solid rocket booster and the liquid fuel upperstage that lifts the CEV into orbit is the Crew Exploration Vehicle Launch Vehicle or CLV. The larger system that lifts the LSAM and other cargo into orbit will be known as the Cargo Launch Vehicle or the CaLV."
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Why Die?
Jim Baen
Note: The author would like to acknowledge the inestimable help received from conversations with Dr Lambshead, and for the enthusiastic support of Professor Eglund, whose analysis follows the article. There are probably several persons on the planet who will understand the analysis.
Many people have suggested that aging is a pre-programmed, genetically controlled function in higher animals. This appears to be confirmed by the research findings of Cynthia Kenyon, an eminently respectable scientist who publishes in peer-reviewed journals, on aging in nematodes. She reported extensions of nematode lifespan of five times normal, i.e. from around two weeks to ten, with their apparent vigour undiminished until shortly before death. In other words, they don’t just drag out old age but function properly for an extended period.
She accomplishes this by selectively blocking the expression of various “DAF” genes, including DAF-2 and DAF-16. DAF-2 suppresses the action of DAF-16, the latter triggers or suppresses at least six other genes the end result of which is to promote longevity. DAF-16 seems to influence the production of proteins that protect against free radical damage. So it could be said that DAF-2 has the function of deliberately limiting a nematode’s life span.
Of course, one has to be careful extrapolating from a nematode worm with a lifespan measured in weeks to something long lived like a human being. In nematodes, DAF-2 and DAF-16 are associated with moulting. Nematodes are Ecdysozoans (moulting animals) and these have the ability to go into a special ‘shut down’ state, known as ‘dauer larvae’ in the case of the Kenyon’s test animal, the nematode Caenorhabditis elegans.
Human beings neither moult nor go into a shut down mode (not even teenagers). However, the DAF-2 gene is similar to a gene in mammals called IGF-1 that is con�
�nected with insulin function. Martin Holzenberger created strains of mice in which one or both copies of the rodent gene for the IGF-1 receptor had mutations. Mice lacking any normal copies died as embryos. However, mice with one working copy developed normally and lived, on average, 26 percent longer than did animals with two normal copies of the IGF-1 receptor gene.
For the purposes of this article, let us assume that getting old and dying is a defined process, a process that is controlled by our genes; that our life span is deliberately limited. Why? This seems astonishingly counter-evolutionary. The two basic driving forces in evolution are (i) survival and (ii) success in mating (for sexual organisms). Surviving by definition implies extension of life span. However, it is also true that for many organisms that the longer an organism survives the more successful it will be at mating - even geeks will manage to reproduce if given enough chances.
So if our life span is deliberately limited by our genes then there must be some evolutionary advantage. The rest of this article will try and address this point.
One possibility is that we limit our lifespan by the need for optimal performance up to the time of successful reproduction. This is the racing car analogy. An engineer designing a Ford or a Peugeot tends to over-engineer to give reliability and a decent lifespan rather than optimise for performance. In contrast, the racing genius Colin Chapman used to examine his cars after a race and any component that was in too good a condition was promptly lightened. An ideal Chapman racing car would fall to pieces one inch after crossing the finish line - but in first place!
The racing car analogy does not really seem to explain Kenyon’s results because when DAF-2 is suppressed the worms stay younger longer; they do not stagger on in senility. It is almost as if the genes do not care how long a worm could live or what condition it might be in through most of that life but just decide it has lived long enough. What evolutionary mechanism could cause this?
In Utah, studies have been done that show that it is possible, in fact surprisingly easy, to track the presence of polygamous marriages by the occurrence of babies with birth defects. It turns out that having a few highly prolific males makes a surprisingly large impact on the occurrence of double recessives in the general population, and that this in turn leads to a surprisingly large number of birth-defects, children with Down’s Syndrome, cleft palate, club feet, various leukodystrophies and the like occur much more commonly than they would without the prior presence of these males. This observation is anecdotally common human experience. Inbreeding causes an increase in nasty recessive genes in the population and polygamy inevitably will increase inbreeding.
This is a common problem in conservation. Once a population of an organism drops below a certain level then the species is in terrible trouble. In theory, one could recreate a species from a single male and female. In practice, there are likely to be enormous genetic issues.
For human populations, inbreeding is likely to be especially dangerous for two reasons. The first is that the human genome is particularly messy compared to other mammals such as dogs or rats. The second reason is that reproductive success of males in human beings (who are highly social animals) tends to be correlated with status and status tends to increase with age. As the hypothetical TV interviewer put to the young blonde, ‘What first attracted you to this elderly, balding, multimillionaire Miss Smith?’ The wealthy middle-aged man with a younger trophy wife is a phenomenon observed in all human society. A long life span in men is more of an issue because one high status man can impregnate many women. Reason one will tend to accentuate the impact of reason two.
So if a meta-population (a subgroup) of a species that has mutations that shorten its lifespan has offspring that are more successful than the offspring of a longer-lived meta-population then the former population will replace the latter. An evolutionary mechanism, therefore, exists that could promote death genes.
Just because this is logical and reasonable does not make it true, but I leave you with one final thought. Women commonly live longer than men and, in my model, it is long lived men that should be more dangerous to the species. If you are male, then nature could have it in for you.
A genetic model for eternal life as an evolutionary strategy
Karl Inne Ugland
University of Oslo,
Marine Zoology
Pb 1066, 0316 Oslo, Norway.
(Portions of the equations of this paper are formatted as graphics which will not render in this format. Please view this paper at the on-line html version or in the PDF’s for correctly formatted equations.)
Introduction
Classical and molecular genetics are concerned with the nature and transmission of genetic information, and how this information is translated into phenotypes. Population genetics theory is most successful when dealing with simply inherited traits - traits whose transmission follows simple Mendelian rules. Yet many of the most interesting and important traits are not so simply inherited: they depend on several genes, which often interact in complex ways with one another and with the environment.
Population genetics includes a large body of mathematical theory; one of the most richest and most successful bodies of mathematics in biology. The useful application of this theory has been greatly enhanced in recent years by new molecular techniques.
Usually, the first step is to study the frequency of different genotypes or phenotypes in a sample of the population. The concept locus is used to designate a chromosomal location, and the concept allele designates an alternative form of the gene occupying the considered position. Usually we are more interested in the frequencies of the different alleles than in the frequencies of the different genotypes. This is because allele frequency is a more economical way to characterise the population. The number of possible genotypes is enormous. Consider for example 100 loci, each with 4 segregating alleles. With 4 alleles A, B, C, D the total number of possible genotypes at each locus is 10: (1) four homozygotes: AA, BB, CC and DD plus (2) six heterozygotes: AB, AC, AD, BC, BD and CD. For all 100 loci there are thus 10100 possible genotypes, i.e. more than the number of atoms in our universe! It is, therefore, much better to stick to allele-frequencies.
The characterisation of a population in terms of allele frequencies rather than genotype frequencies has another advantage. In a Mendelian populati
on, the genotypes are scrambled every generation by segregation and recombination. New combinations are put together only to be taken apart in later generations. If we are to study a population over a time period of more than a few generations, then the stable entity is the gene.
In nature it is the organism that survives and reproduces, so natural selection acts on the organisms and it is the fitness of the organism that determines the likelihood of survival and reproduction. But what an individual actually transmits to future generations is a random sample of its genes, and those genes that increase fitness will be more represented in future generations. Thus, there is selection of genes determining the properties like vigour and fertility.
Any description of nature, whether verbal or mathematical, will only be a caricature and therefore necessarily incomplete. In the previous century, scientists realised that we cannot ask whether a mathematical model is true, we can only ask if it gives a good or bad description of our data, and so may be used for prediction of future observations and experiments. Some models are only rough caricatures, but the advantage with this class of models is that they are easy to understand. An example is the successful theory of thermodynamics where the gas molecules are regarded as elastic spheres.
Jim Baen’s Universe Page 70