But cells with "good" DNA can divide all they want without causing cancer, since they will only do so when the proper signal to do so is present. As you age more and more of your cells will have errors in their DNA (for the reason stated above) that cause them to divide irrespective of whatever external or internal signals to divide or kill themselves. These mutations aren't necessarily the result of faulty DNA replication but can be caused by environmental factors damaging the DNA in a way that isn't repaired correctly which, if it happens at the wrong spot(s), results in altered expression of genes involved in regulating cell proliferation or apoptosis, thus allowing that cell to become cancerous. So what I'm saying is that replication errors aren't the only cause of changes to DNA sequence (your viral theory is an example of this...).
Also the logic behind thinking that more innately proliferative cells are more prone to cancer is also two-fold in that the more times a cell divides the more replications the original DNA will have undergone thus allowing more chances for error (what you seemed to be thinking about) but also DNA packed tightly in heterochromatin is less available to react with whatever chemicals are around to alter it. S-phase DNA is necessarily more exposed to whatever random chemicals are floating around in the nucleus and, throughout the cell cycle, highly-proliferative cells will have those cell division/apoptosis regulating genes more exposed so that they can be easily accessed for transcription and since those genes are normally more active fewer mutations may be unnecessary before you end up with a cell that just grows out of control. Those obviously aren't the only factors though, since, as you say, how often a cell ends up with cancerous progeny isn't necessarily related to how often it normally divides. Maybe it has something to do with accessibility of those tissues to carcinogens or that the ability of the body to detect the faulty cell and/or mount an effective immune response differs by tissue...I don't know, maybe someone has studied it.
Anyway I guess what I'm saying is it doesn't make sense to conclude that cells that divide more become cancerous more often and therefore we should see the same incidence of cancer regardless of age, which is not what happens. Further I don't see how that conclusion supports a viral theory of cancer over chemically induced cancer (oxidative stress, carcinogens). I don't think theres anyone in the know who claims that the primary cause of cancers is errors during DNA replication. I'm obviously ready to entertain the idea that most tumors are the result of viral infection (or else I wouldn't have read what you had to say) but that point you were making still doesn't seem logical to me.
"2. With the sheer number of cells in the human body, late-stage diseases such as cancer should always occur in childhood Your body contains billions upon billions of cells, all replicating, all exposed to free radicals. Except during breastfeeding, your food supply doesn't change much through adulthood. Antioxidants, vitamins, etc, which protect cells should always affect you the same way - you shouldn't need more protection as you get older. It's a limited supply, that needs to be replenished regularly. If you're going to see problems with replication, or other random malfunctions, then they should be as likely when you're young as when you get older. If you're going to get them when you're older, you should get them at the end of puberty if there's any magic involved in still being a child."
---I don't follow this logic at all. Even if the rate of cancer-inducing mutations/epigenetic changes is constant the incidence of cancer should rise exponentially in relation to age since more and more of those mutations will have occurred as time passed.
From your part 3: Apparently HPV does its magic by interfering with the expression of gene P52, a factor in cell death (apoptosis)... Most likely you meant p53, just sayin.
So you worked really hard, beyond expectations, etc. Where did that get you? I mean in terms of eventual success with work, accomplishments, happiness with life, etc. I'm not trying to be cynical, it's just that I'm in grad school (biomed. not CS so not quite the same but still) and have been coming across alot of different attitudes towards how much time/effort one's job needs to take up in order to do something that contributes to society and leaves you satisfied with your effort without wasting your life away working for someone who benefits more from your effort than you do yourself.
Your DNA is actually wrapped around complexes of protiens called Histones and these protiens can be modified to stick together or not. Ones that don't stick together make the genes easy to be expressed, and those that do aren't expressed. This along with modification of the actual DNA making it harder to be expressed (methylation) is what is passed down via the sperm/egg.
OK, well now that I actually read the article its a pretty good one. Anyway heres what is new (at least to me): "the Encode scientists estimate that a staggering 93 percent of the genome produces RNA transcripts"
I would think that the advantage of a strategy that basically amounts to knocking out CCR5 is that there is none of that receptor at all for the HIV to interact with, while using an antagonist is probably never going to saturate the receptor without raising the dose so high that you're going to get side effects somewhere, which leads me to a couple questions (my immunology is severely lacking). 1) Where are T-cells located (ie in the bloodstream, in connective tissue, etc)? What happens to HIV if it doesn't find a host cell and how long does this take (ie whats a single virons usual lifespan in a host, do they end up clogging up capillaries, do they somehow migrate out of the blood vessels)? I mean does it make sense to think a combination of a CCR5 antagonist and siRNA for CCR5 would result in few enough Virons being successful that they would get degraded in a reasonable time span after using up all available hosts?
I read Jurassic Park around 6th grade, then got into his other stuff. Looking back he was probably the primary influence in terms of getting me into sci-fi and eventually wanting to become a scientist.I guess that could be good or bad depending on how you look at it. I've still got time to accidentally kill off 99 percent of the worlds population.
Listen to parent, the tv remake was one of the most retarded things I've ever seen. For example, the whole multilevel decontamination procedure was replaced by what looked like a rave party with everyone dancing through foam with lights strobing.
I'm really for helping people out but if you go skiing or (insert risky activity here) and fuck yourself up an ideal system would make you pay for it yourself, because however much your skiing and having fun could have improved my life is so indirect that it'd be impossible to prove if it did or not and I'd rather not pay for it.
Yea they wait until the animal is sleeping then bite. Also I don't know if it was in this article or the NY times one posted somewhere here that said the spit also has some sort of painkiller in it.
would have been how the bats manage to avoid becoming haemophilic despite constantly secreting and ingesting a plasminogen activator, especially one resistant to inhibition. I mean not all of the protein is going to be be broken down before absorption. I'm not sure what the kinetics of the bat PA are like but Id imagine a low concentration could activate alot of plasminogens since you usually want your blood to clot pretty fast after getting cut.
So in your metaphor America is a battered wife while al queda (or whoever you want as the enemy) is the drunken asshole husband? Thats a pretty terrible metaphor.
Interesting... I just realized I don't know enough about the electronics involved to figure that one out without spending a day on it but someone else should propose a theory
Slashdot Mirror
But cells with "good" DNA can divide all they want without causing cancer, since they will only do so when the proper signal to do so is present. As you age more and more of your cells will have errors in their DNA (for the reason stated above) that cause them to divide irrespective of whatever external or internal signals to divide or kill themselves. These mutations aren't necessarily the result of faulty DNA replication but can be caused by environmental factors damaging the DNA in a way that isn't repaired correctly which, if it happens at the wrong spot(s), results in altered expression of genes involved in regulating cell proliferation or apoptosis, thus allowing that cell to become cancerous. So what I'm saying is that replication errors aren't the only cause of changes to DNA sequence (your viral theory is an example of this...).
Also the logic behind thinking that more innately proliferative cells are more prone to cancer is also two-fold in that the more times a cell divides the more replications the original DNA will have undergone thus allowing more chances for error (what you seemed to be thinking about) but also DNA packed tightly in heterochromatin is less available to react with whatever chemicals are around to alter it. S-phase DNA is necessarily more exposed to whatever random chemicals are floating around in the nucleus and, throughout the cell cycle, highly-proliferative cells will have those cell division/apoptosis regulating genes more exposed so that they can be easily accessed for transcription and since those genes are normally more active fewer mutations may be unnecessary before you end up with a cell that just grows out of control. Those obviously aren't the only factors though, since, as you say, how often a cell ends up with cancerous progeny isn't necessarily related to how often it normally divides. Maybe it has something to do with accessibility of those tissues to carcinogens or that the ability of the body to detect the faulty cell and/or mount an effective immune response differs by tissue...I don't know, maybe someone has studied it.
Anyway I guess what I'm saying is it doesn't make sense to conclude that cells that divide more become cancerous more often and therefore we should see the same incidence of cancer regardless of age, which is not what happens. Further I don't see how that conclusion supports a viral theory of cancer over chemically induced cancer (oxidative stress, carcinogens). I don't think theres anyone in the know who claims that the primary cause of cancers is errors during DNA replication. I'm obviously ready to entertain the idea that most tumors are the result of viral infection (or else I wouldn't have read what you had to say) but that point you were making still doesn't seem logical to me.
also, regarding the following:
"2. With the sheer number of cells in the human body, late-stage diseases such as cancer should always occur in childhood
Your body contains billions upon billions of cells, all replicating, all exposed to free radicals. Except during breastfeeding, your food supply doesn't change much through adulthood. Antioxidants, vitamins, etc, which protect cells should always affect you the same way - you shouldn't need more protection as you get older. It's a limited supply, that needs to be replenished regularly.
If you're going to see problems with replication, or other random malfunctions, then they should be as likely when you're young as when you get older. If you're going to get them when you're older, you should get them at the end of puberty if there's any magic involved in still being a child."
---I don't follow this logic at all. Even if the rate of cancer-inducing mutations/epigenetic changes is constant the incidence of cancer should rise exponentially in relation to age since more and more of those mutations will have occurred as time passed.
From your part 3: Apparently HPV does its magic by interfering with the expression of gene P52, a factor in cell death (apoptosis)... Most likely you meant p53, just sayin.
No... its not just any coincidence.
Mod lysergic acid interesting.
So you worked really hard, beyond expectations, etc. Where did that get you? I mean in terms of eventual success with work, accomplishments, happiness with life, etc. I'm not trying to be cynical, it's just that I'm in grad school (biomed. not CS so not quite the same but still) and have been coming across alot of different attitudes towards how much time/effort one's job needs to take up in order to do something that contributes to society and leaves you satisfied with your effort without wasting your life away working for someone who benefits more from your effort than you do yourself.
Nevermind they were just talking about transcription factor binding sites. None of this is new stuff.
Your DNA is actually wrapped around complexes of protiens called Histones and these protiens can be modified to stick together or not. Ones that don't stick together make the genes easy to be expressed, and those that do aren't expressed. This along with modification of the actual DNA making it harder to be expressed (methylation) is what is passed down via the sperm/egg.
OK, well now that I actually read the article its a pretty good one. Anyway heres what is new (at least to me): "the Encode scientists estimate that a staggering 93 percent of the genome produces RNA transcripts"
At least I've got a plan... So what's yours?
Epigenetics
RNA Splincing
siRNA
Well for HCl you just cut open the stomaches of all the monsters victims and gather the juices then throw it on him, at least thats what I'd suggest.
I feel like I caught a glimpse of one of the Great Old Ones or something
PERVERT!
I would think that the advantage of a strategy that basically amounts to knocking out CCR5 is that there is none of that receptor at all for the HIV to interact with, while using an antagonist is probably never going to saturate the receptor without raising the dose so high that you're going to get side effects somewhere, which leads me to a couple questions (my immunology is severely lacking). 1) Where are T-cells located (ie in the bloodstream, in connective tissue, etc)? What happens to HIV if it doesn't find a host cell and how long does this take (ie whats a single virons usual lifespan in a host, do they end up clogging up capillaries, do they somehow migrate out of the blood vessels)? I mean does it make sense to think a combination of a CCR5 antagonist and siRNA for CCR5 would result in few enough Virons being successful that they would get degraded in a reasonable time span after using up all available hosts?
Wake you up and charge you 9 million dollars for a pint?
You mean the Doppler 2000?
I read Jurassic Park around 6th grade, then got into his other stuff. Looking back he was probably the primary influence in terms of getting me into sci-fi and eventually wanting to become a scientist.I guess that could be good or bad depending on how you look at it. I've still got time to accidentally kill off 99 percent of the worlds population.
Listen to parent, the tv remake was one of the most retarded things I've ever seen. For example, the whole multilevel decontamination procedure was replaced by what looked like a rave party with everyone dancing through foam with lights strobing.
I'm really for helping people out but if you go skiing or (insert risky activity here) and fuck yourself up an ideal system would make you pay for it yourself, because however much your skiing and having fun could have improved my life is so indirect that it'd be impossible to prove if it did or not and I'd rather not pay for it.
Your job sounds awesome.
Yea they wait until the animal is sleeping then bite. Also I don't know if it was in this article or the NY times one posted somewhere here that said the spit also has some sort of painkiller in it.
would have been how the bats manage to avoid becoming haemophilic despite constantly secreting and ingesting a plasminogen activator, especially one resistant to inhibition. I mean not all of the protein is going to be be broken down before absorption. I'm not sure what the kinetics of the bat PA are like but Id imagine a low concentration could activate alot of plasminogens since you usually want your blood to clot pretty fast after getting cut.
So in your metaphor America is a battered wife while al queda (or whoever you want as the enemy) is the drunken asshole husband? Thats a pretty terrible metaphor.
Interesting... I just realized I don't know enough about the electronics involved to figure that one out without spending a day on it but someone else should propose a theory