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Tumor-suppressing Gene Contributes to Aging
Van Cutter Romney writes "Scientists have discovered a tumor suppressing gene which also leads to aging in stem cells. The gene also known as p16INK4a when removed from 'knockout' mice resulted in older mice having organs as healthy as younger ones. However they didn't live any longer than normal mice. The new study was confirmed by three independent researchers from Harvard, UNC Chapel Hill and University of Michigan."
"I don't think aging is a random process - it's a program, an anti-cancer program,"
Cancer, then, is an anti-aging program.
The article basically states that when they turned off the flow of ink-4, embyyonic stem cells were free to divide without check. The mice without the ability to produce ink-4 developed cancer within a year and died. This behavior cannot be reliably reproduced in aged stem cells, and ink-4 production naturally increases exponentially with age.
The main news I see here is either a possible avenue for cancer research, or a good supporting argument to lift bans on exploiting new strains of embryonic stem cells (over adult stem cells). This does not represent a specific breakthrough, but yet another amazing revelation of stem cell capabilites has come to light.
I support the ban on cloning, I disagree with the ban on new stem cells, I am relatively opposed to mass abortion, but banning it would be stupid. I think this story's new information supports these views.
FairTax baby!
Isn't this talking about the same thing as this article: http://science.slashdot.org/science/05/04/06/23302 49.shtml?tid=191&tid=14
which was posted here over a year ago?
I guess this is pretty good for slashdot to go over a year without reposting a similar story.
although it does not follow directly from this discovery, is the question: If you could change the balance at any point, what would it mean to be able to choose between heightened risk of cancer and some of the worse effects of old age? What a choice to have to make. (AFAIK, this is not even an issue, just something I thought of after hearing of it. I did not RTFA, but I heard this same discovery reported on the news recently.)
You live and learn. At least, you live.
If the organs in the older mice were just as healthy as those in younger mice, how did they not live longer? It would seem to me that if your organs are perfectly healthy, you'll live. Wonder what the catch is.
The heavens do not fall for such a trifle.
The article basically states that when they turned off the flow of ink-4, embyyonic stem cells were free to divide without check. The mice without the ability to produce ink-4 developed cancer within a year and died.
There's a famous principle in Mathematics & Quantum Mechanics, first discovered by the British mathematician GH Hardy, and then refined by Heisenberg, which states that both a function & its Fourier transform cannot decay too rapidly [otherwise the function is identically zero].
Or, as Mic Jagger put it: You can't always get what you want.
So it sounds like The Designer of the Universe [a pretty intelligent Fellow, from what I hear] may have placed the very same restrictions on the stuff He created on Day 5 as He did on the stuff He created way back on Day 1.
From what I know about cancer, which isn't a whole lot, the immune system is supposed to be a supressor of tumors. It doesn't make any sense for just a gene to do it if it isn't one related to white blood cell manufacturing. To make a long story short, the "cancer supressing" powers of the gene are barely noteworthy, like putting on a spring jacket to stop frostbite at -40 F, and they wrote it in that biased way so it makes a dramatic headline that implies you may have to choose between living longer and an increased risk of cancer.
now stop reading and go play Dance Dance Revolution!
Support, with data, that Republicans "have barely a high school education" or "may not have taken even the most basic high school-level introductory classes to biology.
You will find that the distribution of ignorance, indifference, stupidity, pandering, sloth, envy, ambition, hatred, disgust, and pretty much any adjective--positive or negative--can be applied universally to any politician or political person regardless of affiliation.... PLEASE PLEASE PLEASE don't let (force) a really good discussion that THE WHOLE WORLD WILL READ degrade into US partisan politics, you [explicative].
FairTax baby!
I think you fail to understand the possibilities of having multiple avenues for the body to prevent unchecked cellular reproduction. Built into each cell should be the codings to tell it how and how often to divide, and at what stages of life. When those checks fail due to any number of circumstances (mutations due to environment or flawed genes), a secondary check, the immune system, responds to a threat of unchecked cellular reproduction by destroying it if possible.
Think of it like social behavior. Ideally, all pro-social behavior is internalized and you operate within the guidelines of the law. However, when you fail to (speeding, for instance), law enforcement is there to step you back into the proper action.
The gene probably slows metabolism. Slower metabolism means fewer chances of cell replication errors, reducing the risk and spread of cancer. It has been speculated for about the last 10 years or so that there is a trade-off between slowing of aging and cancer risk.
This is probably why a handful of humans had deseases causing them to age far too prematurely, but NEVER the opposite (at least not on a signif scale). Thus, entropy is innevitable it appears. Errors happen. Either we slow down to death or get innundated by cell replication errors to death. Same end.
Table-ized A.I.
It's all the unremarkable things that will eventually add up to a tool to fight against, or a cure for cancer. DNA FTW.
FairTax baby!
Actually, genetic safeguards are potentially more important than immune response in many ways.
The immune system is handicapped by the fact that with at least some types of cancer, there is comparatively little difference between the malignant and healthy cells. If it can't tell them apart, it can't stop the cancer from developing or spreading. You're right in that the immune system can sometimes stop cancer, but from a survival standpoint it's better not to get it in the first place.
So we have genes in place to limit cell replication. It's been suggested that aging is an inevitable side effect of these limits (take a look at telomeres for instance). Just the immune system by itself, or just the genetic protections by themselves, isn't enough; you really want both defenses.
Oversimplified, the genetic element is why some cancers run in family lines, and the immune element accounts for why some cancers develop when the immune system is weakened (like KS in AIDS patients).
Erotic is when you use a feather. Exotic is when you use the whole chicken.
Yes, when cancer works, you stop getting older.
Q.E.D.
This issue is a bit more complicated than you think.
That has very little to do with the immune respose issue you mention, which comes in significantly later, when tumors have actually started to form. The oncogene / tumor suppressor interactions are part of the balance that allows normal, but not abnormal, growth.
What I'm listening to now on Pandora...
I can agree with your statement that, "Republicans will likely do their best to block such research." However, from what source did you find "that many of these Republicans have barely a high school education." Surely Sen. Frist, the Senate majority leader who also has an M.D., had to have taken "basic high school-level introductory classes to biology." But as far as the Republicans limiting the US's "ability to take advantage of the upcoming developments and discoveries [in stem cell research]" - I find that unlikely. One, the states themselves in some cases have approved funding for stem-cell research. Two, I personally find it unlikely that the Republicans will control both the legislature and Presidency in the coming years.
Don't worry about the mule, just load the wagon.
okay, I'll explain it a bit more. What I'm 99% sure they're referring to is a gene that affects how much of a certain mollecule (or maybe group of mollecules) is chopped off when a cell splits. It's a little barbel shaped thingy and every time a cell divides, it loses a little bit of it. Once it's out, the cell can't divide anymore and it dies. Cancer cells are defined by having unlimited barbels. They never run out so it divides over and over and never stops. Remove this gene and your cells can split significantly more times before the barbel runs out, thus the extended life. But, they say that this gene can sometimes inhibit cancer cells from growing out of control. The chance that this gene would be powerful enough to reduce the barbel on a cancer cell are astronomical. If it was really even close to an immunity to cancer, you'd practically have progeria because it would take so much barbel limiting power that regular cells would have a very low diving limit.
Btw I lied when I said I didn't know much about this cuz I've seen a show and science class movie about it.
now stop reading and go play Dance Dance Revolution!
Does the same thing apply to a cell?
In other words, as a cell ages is it more likely to have a cancerous mutation? And how does this likeliness compare to the chance of having a cancerous mutation through a cell's reproduction process? (these are for the biologists out there)
If you have a greater chance to have the mutation a cell reproduces then you'd want cells to live along time so they have to reproduce less. If you have a greater chance as the cell sticks around (ages) then you'd want more reproduction and a shorter life span (even though this would be less energy and resource efficient, but maybe more efficient than fixing/killing cancerous cells).
I heard this on NPR today...I was wondering why they didn't say "Aging gene surpresses tumors"...
ZuluPad, the wiki notepad on crack
I think you are correct that the tides are turrning as far as I can see. State funding is still meager right now, not nearly enough for such a valuable, life-affirming effort as stem cell research. And in the past five years many many many millions of people have possibly had their terrible fate sealed by the current administration.
About the other point. I'm sure Frist was a wonderful heart-surgeon. But he's not the type of doctor that I want operating on my heart, considering he renders life or death medical decisions with scant evidence and apparently considering only the impact it will have on his preconceived, unscientific, political and religious "pro-life" agenda.
An M.D. doesn't mean much if you can't observe the clear difference between a person clearly in a persistent vegetative state and a person who still has high-level brain function - the Terri Shaivo case being the thing I have in mind.
So while the poster was exaggerating, it appears that there is a systemic problem with thinking, reasoning, and making objecive reasoning based on the facts - all skills that should have been learned in high school.
"and making objective decisions" was the thing I meant there.
Perhaps I should have paid better attention in English class.
Imagine youthful looks and good health almost all your life, then dying of cancer before you hit 80.
Knowledge is how to play a game, intelligence is how to win, wisdom is knowing what game to play.
And what exactly are your credentials to make such a judgement? Are you a cancer researcher? A doctor? A secretary at a cancer treatment center? Or are you just pulling stuff out of your ass?
WHat you are saying is "I dont know a thing about cancer, but from what I have heard from random gossip, these highly trained profesionals who have staked thier careers on their published findings in a reputable medical journal have no idea what they are talking about."
The first thing that needs to fail is the proofreading enzymes, so that a gene or two are damaged without being repaired.
Then the "self destruct" needs to fail to activate in a cell, The self destruct is almost always armed and ready to go, unless it gets knocked out by a "lucky" mutation.
Even if the self destruct fails, the cell sensing needs to fail in order to grow beyond a few cells. Then the telemorase halting needs to fail in order for the cancer to reach something larger than a mole.
The immune system is a last resort, and not a very good one in comparison.
Storm
Sorry, have to point out a few things, though I'll generalize just a little bit: at the cellular level, metabolism references the processing of energy which is almost wholly seperate (and outside of the nucleus) from the machinery that engages in the correction of dna replication errors. All cells die, whether it's by "old age" or apoptosis (programmed, organized cell death brought on by problems detected at checkpoints during the cell cycle--as opposed to necrosis due to an injury which we'll ignore for this discussion) and these are actually good things for the organism (us humans in this case). Replication errors happen, but our cells are VERY good at detecting and correcting it...it actually takes much more to go from an error in the cell to a cancer within a human (6 things actually): self-sufficiency in growth signals, insensitivity to anti-growth signals, evasion of the aforementioned apoptosis, unlimited replicatability, sustained angiogenesis, tissue invasion and metastasis. It is these that a potential tumor cell must overcome in order become cancer as we commonly know it.
To tie all this into TFA, they were dealing with one aspect of avoiding anti-growth signals; beating aging through this route while still keeping a lid on uncontrolled (cancerous) growth is not necessarily impossible. As for the knockout mouse model used, just look at them wrong and a tumor pops up...
One key mistake in the parent's summary: Ink-4 limits the ability of adult stem cells to divide. The article suggests a theory that because damaged adult stem cells are prevented from dividing by Ink-4, unchecked tumor growth (cancer) is averted later in life.
How this supports embryonic stem cell research is: we now have evidence that adult stem cells will not be effective when used as treatment because they will be naturally suppressed. Thus to get stem cells that will divide and provide therapy, we must use embryonic cells.
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I agree that it is unnecessary to call out one political group and to globally label members of that group inept and incompetent. It is a separate question entirely to judge the education of all members of government and the extent to which this informs their decision making.
But, it has been partisan politics that has interfered greatly with science for quite some time now. In particular, politicians have been bent to the will of religious groups. Yet these same groups daily depend on the fruits of science, engineering and technology for their existance. It's a cafeteria approach - they want to be able to lord over science as they see fit and coerce politicians to force a policy consistent with *their* views. This is not the way of science. Science is secular and depends crucially on adherence to the scientific method.
The relevant point made in that post is that other countries will in fact not hold themselves back with stem cell research. The breakthroughs will happen outside US soil. US citizens with means will continue to travel outside their border to seek treatment not available in their own country. One also wonders if US trained scientists will become fed up with tightening scrutiny of their work and simply themselves immigrate elsewhere to continue research as well. Although this seems preposterous given the high caliber of the US university system and laboratory facilities, I don't see it out of the realm of possibility.
anyone else is seing nintendo logos everywhere on /. ?
The best test environment is production. - Me
chrome://browser/content/browser.xul
In the western world old people are sitting in their big houses with backyards while young families with children are crowded into small apartments.
Once the old people can no longer look after themselves, they will be put into a care home, and kept alive for decades using modern technology. I visited old folks homes for a while, and me playing chess with an old man for 1 hour a week was the highlight of his life, the highlight for another man was me rolling a ball back and forth on a table to his arthritic hands - it made me incredibly depressed.
It seems that living longer, no matter at what quality of life, is regarded unquestioningly as a good thing. People can and do suffer when they are old, and if they want to die, the state will not allow them that choice.
Old person: "I don't want to live, I am in immense pain"
Government: "You are not allowed to end your suffering, we will force you to stay alive and in pain"
Keeping people alive has a cost. Every old person living in a semi-comatose state in a nursing home has costs to the person, the country and the world, the same amount of money could probably save 5-10 dying children in a developing country.
All I'm saying is, maybe we should think about quality of life rather than quantity.
In this present work, it is a gene that, in a way, computes a differential equation--weighing the importance of replacing cells using stem cells from its cache against the risk that the replication of cells will result in a cancerous cell. "To offset the increasing risk of cancer as a person ages, the gene gradually reduces the ability of stem cells to proliferate."
If I understand it correctly, this is a SLIGHT mischaracterization. It's not about risk of creation of cancer cells so much as it is about limiting tumor size - generally in malfunctioning differentiated cells - and limiting stem cells is an undesirable side-effect of how it's done (though it WOULD also limit a stem-cell tumor, if such exist).
The mechanism (or set of mechanisms) is a limit on how many times a non-gamette cell may replicate. Thus when a cell mutates so that it, and its progeny, continue to replicate (ignoring their normal limits), the resulting tumor reaches a maximum size (say-pea sized) and stops growing. (It may even die off, as cells die TRYING to replicate with an "expired meter", or are no longer replaced fast enough to stay ahead of immune-system attacks).
The smaller the tumor when it hits the limit, the better (and the less likely some cell within it will acquire the ADDITIONAL mutations necessary to escape this limit, founding an "immortalized" tumor cell line). But there's the downside that the limit also results in cellular senescence - inability of the body to replace tissue in late age, because the "counter" in the otherwise-fine cells is running out.
So the limit apparently evolves with the typical lifespan of the population, allowing enough replication that cellular senescence doesn't begin to occur in normal inividuals until virtually all of them would be dead (or otherwise no longer an asset to the species) due to other causes. (I vuagely recall reports of research suggesting the typicall setting is something like twice as many cell replications as are necessary to avoid senescence by the age where about 95% of the population would be dead.)
Meanwhile other protective mechanisms (such as the metabolically-expensive production of antioxidant enzymes) co-evolve to trade off keeping the cancer rate down against resource consumption, given the typical lifespan due to risks and the cell-reproductive limit setting. (THESE are the "twiddle settings" that trade off CREATION of a cancer cell against other life-shortening factors.)
The settigs of these protective mechanisms apparently evolve quite rapidly, so they tend to closely track the lifespan-due-to-circumstances of most species that have been in their niche for a while. But the human lifespan has been drastically extended in a period that is evolutionarilly VERY short, thanks to weapons (protection against predation and improved hunting success), agriculture, animal domesitication, lore transmission, medicine, and other technological and cultural improvements in lifestyle. So plenty of people live to the "threescore and ten" or so years when the current setting of the cell replication limit tends to cause fatal system failures.
Research such as this, identifying the details of the mechanisms, should lead to interventions to compensate for the now incorrectly-low setting of this "tuning knob" in the human genome.
Bantam Dominique roosters crow a four-note song. Once you've heard it as "Happy BIRTHday" you can't NOT hear it that way
So, if I understand it correctly, if we were able to prevent cancer (by finding a root cause or otherwise), then that would change the risk equation balanced by this gene. This gene could then be turned off, the effect of which would be unabated rejuvenation of body organs, leading to indefinite lifespan.
"There is no free lunch -- we are all doomed," Dr. Sharpless said. But he quickly modified his comment by noting that a calorically restricted diet is one intervention that is known to increase lifespan and reduce cancer, at least in laboratory mice.
Unfortunately, caloric restriction only raises the life expectancy of rodents in the laboratory, not when exposed to natural conditions. While it reduces risk of cancer, it also drastically reduces the effectiveness of the immune system at fighting off infection (and the resulting stresses which, in turn, re-raise the cancer risk.)
This has been known for decades by those educated in food & nutrition science. Unfortunately, the news has apparently not spread widely in other fields.
So while there is a strategy that reduces both of these TWO problems, it does it at the cost of creating a third. Again no free lunch.
Though there may be useful insights from the lab results, life extention strategies based on caloric restriction in the real world seem unlikely to be successful.
Bantam Dominique roosters crow a four-note song. Once you've heard it as "Happy BIRTHday" you can't NOT hear it that way
Your body maintains enough cell division activity to do upkeep, but obviously, there are limits to that- the slow deteriorations of age, as well as the inability to make certain repairs. If p16-Ink4a is not there to inhibit its target, the kinase it inhibits will give the "go-ahead" to the cell to replicate its chromosomes, divide, return to that checkpoint, replicate, divide, and so on. If the several cell systems whose function it is to notice this alarming occurence fail in their task (your cells have genes which try to initiate suicide in the cell if an error is detected), then the cell divides out of control- cancer. This is at the very beginning of a cancer, and all happening inside the tumor cell- the rest of your body is not on alert yet. Basically, if p16-Ink4a is working correctly, it prevents cells from ever becoming cancer in the first place. The relationship to stem cells is quite interesting as well- through the action of this gene, your body essentially makes the decision that as you age, keeping around active stem cells to maintain your tissues is not worth the increased risk of cancer they represent.
"FDA staff reviewers expressed concern about the number of patients who were left out of the study because they died."
Perhaps you're thinking of the antediluvian patriarchs. Noah was one of the younger ones at like 600.
I cried real tears when Li Mu Bai died.
Anyway, it's an important distinction to make; a cell's chance of mutation doesn't always just stay at [arbitrary %], rather, the odds increase with time.
Sony ha
Research now shows that tumors and cancers help stop the aging process altogether, unfortunate side effect is death.
Unfortunately, caloric restriction only raises the life expectancy of rodents in the laboratory, not when exposed to natural conditions. While it reduces risk of cancer, it also drastically reduces the effectiveness of the immune system at fighting off infection (and the resulting stresses which, in turn, re-raise the cancer risk.)
/ 09/calorierestriction.php
This has been known for decades by those educated in food & nutrition science. Unfortunately, the news has apparently not spread widely in other fields.
It all depends how you do it:
http://www.genomenewsnetwork.org/articles/2004/07
I am following a lakto-ovo vegetarian lifestyle myself, and can't really say that I'm missing flesh at all. Combine it with drinking lots of water, and your body will become VERY healthy. You will notice the difference within weeks.
However, key to a good diet is enough proteins. Too many young girls start eating only pizza, salads, pasta, etc. and get malnutrition as a result from going "veggie". A veggie-diet without enough proteins and variation is no veggie-diet in my book. Correct veggie recepees have been used for thousands of years in the East, based on the Vedic Science of Ayur-veda (knowledge about life).
Btw, what is the point of extending your lifetime, if you're miserable? Quality time, living here and now, is much more important than the length of your life - which is only fear of something so natural as death.
http://www.debunkingskeptics.com/
http://www.cell.com/content/article/abstract?uid=P IIS0092867402008188
I spot a trend here ;-)
No. living longer != aging Aging is the deterioration of the body due to a lack of cell growth. anti-aging would therefore cause a better quality of life. Right now (as you put it), people are living longer, and are aging... It is this aging that is causing them to have poor quality of life. Granted, if they had a shorter life, they wouldn't age as much. But if we had anti-aging, people would live longer AND not age, thusly quality of life would be quite good. This study suggest that the aging process (or the lack of cell growth) is to combat the growth of cancerous tumors. by turning off ink4, the mice did not age... but coincidentally lived the same amount of time due to cancer. If the person
"Infecting minds with my own memetic virus, one post at a time." Ultimape
So, it is not that there is a gene that causes cancer, its that some people are lacking genes which prevent cancer... But, what if there was a gene that causes cancer, and a one that prevents it. Could there perhaps be a darwininesque situation within the gene pool itself, with genes fighing amongst genes. With each generation, not only are we evolving, the genes themselves are having mini evo battles, whose micro-turbulence causes macro-turbulence within the species. It would be a system set up so that genes evolved a way for genes to evolve quicker than normal. So perhaps cancer is itself both a blessing and a curse, it helps thin out the species only to allow more room for the speices to grow. Oh the beauty that is the edge of chaos. we could win the battle, but lose the war, so to speak.
"Infecting minds with my own memetic virus, one post at a time." Ultimape
Woosh! The sound of a Heisenberg/TANSTAAFL joke flying right over your head.
This article is actually related to this article.
The scientists in the article I linked to were using this guy's findings to test ways to engineer controls on this particular gene that would allow it to be used to attack cells that overproduce and shut them off.
Basically, they can't just shut it off to stop aging in the sense of the inevitable march toward death, but they can do two other things:
1) Engineer the cells so that as you get older chronologically you do not get older biologically (ie you won't live any longer, but you'll live a lot better).
2) Engineer a sort of "antibody cell" specific to each cancer patient that can be used to target problem cell divisions specifically while also eradicating the more general problem it has created in the surrounding area using current chemo techniques.
If this were true, every baby born would be one huge cancer tumor. You can't create a sperm or egg without "letting cells divide"; if that inevitably led to cancer, the human race would die out in just a handful of generations.
Personally, I don't believe "immortality" is possible for people; but all life on earth depends upon cellular immortality.
"What's even more disappointing, however, is that many of these Republicans have barely a high school education."
Sorry, but when the subject of your point ('of these Republicans') can be easily replaced with an asterisk, your point suffers. For example, I could replace it with 'inteliigent designers', 'radio pundits', or 'of the citizens of pennsylvania', and it would still be true.
That doesn't make it a point. It makes it astroturfing.
110100 1101000 1101000 1100110 0 1101111 1101000 1100011 1
Do these stemcells we're reading about include the telomeres that act like "time to live" cell division countdown timers in cells' DNA? Do embryonic stemcells have more generations left in them than do more adult stemcells?
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make install -not war
It's called antagonistic pleiotropy http://en.wikipedia.org/wiki/Antagonistic_Pleiotro py. The fitness curve at it's simplest has a central maximum, and drops off towards the extremes. The location of the maximum will depend on a number of things - for one examination see http://medbiograd.sa.utoronto.ca/pdfs/vol2num1/10. pdf (page down to the start of the article)
So, Mick Jagger is an alien, QED.
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The summary says: However they didn't live any longer than normal mice.
This isn't really surprising. I think that JSB Haldane provided the mathematical framework for showing why this is the case.
First off, evolution is about amplification: the genes from an animal that has more children, younger, will be spread more than the genes from an animal that lives longer, so the successful strategy is to commit energy towards early maturation, rather than towards longevity.
Secondly, and this is the part Haldane worked on, if there are multiple systems that contribute to aging, they will, over time, have their age-related effects converge. The system that leads to the earliest death-from-old-age is the limiting factor, and will have pressure (assuming the animal is still of breeding age) to stretch longer, while any other senescence-related systems will tend to shorten to minimize energy expenditure, until they all have roughly the same value. It becomes a weakest-link-in-the-chain situation, where removing one limiting factor just exposes another with roughly the same limiting value. That's a messy summary of the original theory, but it's been a decade since I read a lot about this: sorry.
Nostalgia's not what it used to be.
p16INK4a
I mean, not only did it take me a minute to parse, it, I have no idea what Oiginkaa is.
Please stop stalking me, bro.
You can't draw that conclusion without knowing the pathways involved in expression of INK4.
Extracellular signalling pathways, such as G-coupled protein receptor pathways, may be key to INK4 expression levels. If that is the case, embryonic stem cells would likely undergo the same INK4 suppression as adult stem cells, whether they be transplanted or naturally occuring.
The key is then not the source of the stem cells but modulation of protein expression in the stem cells you have.
Republicans and conservatives generally tend to fall into the middle intelligence range. The stupid tend to be poor and want someone to take care of them, which is not Republican politics. The very smart tend to be highly educated; those with many years of college are worn out by constant exposure to the highly liberal educational "elite". Eliminate these extremes and unmarried women, and you have a Republican majority.
Contribute to civilization: ari.aynrand.org/donate
It is ironic that you are willing to make such enormous logical leaps given your user name.
I was merely representing TFA in the comments. The gp made an error in summarizing the content of the article, so I tried to make that clear. Opinions and logic expressed were that of the article.
Frankly, I find it ironic that you're trying to draw conclusions about a user name that, in itself, contradicts anything you might come up with anyway.
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Frankly, I was making a joke.
Now who's joking?
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