Favorite Nonfiction Science Books
The Cosmic Serpent: DNA and the Origins of Knowledge (by Jeremy Narby)
The Holographic Universe (by Michael Talbot)
Life's Other Secret: The New Mathematics of the Living World (by Ian Stewart)
The Elegant Universe: Superstrings, Hidden Dimensions, and the Quest for the Ultimate Theory (by Brian Greene)
Quantum Evolution: The New Science of Life (by Johnjoe McFadden)
Quantum Brain: The Search for Freedom and the Next Generation of Man (by Jeffrey Satinover)
The Shifting Realities of Philip K. Dick: Selected Literary and Philosophical Writings (by Philip K. Dick and Lawrence Sutin)
The Web of Life: A New Scientific Understanding of Living Systems (by Fritjof Capra)
Favorite Sci-Fi Books
VALIS (by Philip K. Dick)
Nova Express (by William S. Burroughs)
Labyrinths: Selected Stories and Other Writings (by Jorge Luis Borges)
Flow My Tears, The Policeman Said (by Philip K. Dick)
A Scanner Darkly (by Philip K. Dick)
Favorite Sci-Fi Movies
2001: A Space Odyssey
Blade Runner
Pi
Delicatessen
Metropolis
Favorite Subjects
Quantum Consciousness/Communication
Crude Analogy: The mainstream scientific understanding of neurobiology is equivalent to the time period before we had the mail system or telephones...you could only talk to someone if they were near you. Now we can write an e-mail message and talk to someone on our cell phone at the same time. In other words, we can talk to people non-locally (at a distance) and instantaneously (in parallel). This is controversial, but perhaps the neurons (nerve cells) or all cells in our body communicate like people do today.
This is the idea that quantum events play a large role in our consciousness...integrating quantum mechanics, neurobiology, and quantum computers...and even DNA into one continuous whole.
Experimental Evolution
Crude Analogy: Imagine you could thaw out several vegetarian dinosaurs from the freezer and allow them to compete with several hard-core vegetarians (the evolved form of a Stegosaurus, just pretend) at the salad bar and see who would have better fitness - who can reproduce more offspring in a certain environmental context - in the salad bar (assuming the generation time is the same for both dinosaur and vegetarian).
This is what Stephen Jay Gould calls, "some of the most exciting stuff in evolution," for good reason...you can watch how bacteria evolve literally before your eyes in a certain environmental context (or in "normal" laboratory growth conditions after altering its DNA content - how do the cells adapt?). Then you can do competition experiments (for fitness - how well will the cells grow?) between the evolved bacteria and the ancestral form (the original bacteria before exposing them to that certain environmental context - like at a low temperature, for instance). The bacterial strains (having a characteristic DNA sequence) with the highest replication rate (and hence can probably divide the fastest) might not always be the winners, you know. If you end up with one or a small number of really fast replicators and a bunch of semi-fast replicators, then perhaps the semi-fast replicators will have the numbers to outcompete the fast replicators in the future. This is because there might be a trade-off to being a fast replicator. One example might be that the semi-fast replicators are very "robust" when they accumulate mutations and so they are less likely to be affected by deleterious mutations compared to the fast replicators. Also, in this system you can discover how bacteria evolve naturally (well, almost naturally since usually bacteria in nature exist in biofilms or communities) and try to figure out how and why the mutations are deleterious, neutral, advantageous, or compensatory (possibly compensating for the deleterious mutations) - a form of an advantageous mutation. This is the perfect experimental setup to study long-term evolution and adaptation in microbes to give us possible answers to subjects such as antibiotic resistance (see below), adaptive evolution (see below), and cancer.
Antibiotic Resistance
Crude Analogy: If you could see a bacterial cell or virus, would you use every weapon possible to kill it or just one? Would you fire 6 shots or only 5 [smirk]? It seems intuitive to use all the weapons you could, but not if germs are incredibly adaptive (which they are). Even though you will kill a large percentage of germs with a gun, knife, hand grenade, rope, radiation, toxic gas, and a Mac truck, a few will survive and say, "Thanks, now I'm a super germ, will propagate, and will soon kick your ass!
This is an ever-increasing problem because it has been found that bacteria and viruses around the world are resistant to several antibiotics (many of these are common drugs). Why is this a problem, you say? Because antibiotics work to kill a good majority of the bacteria so that your immune system can take care of the rest. Normally this is not a problem because your own immune system is quite adaptive itself. However, if your immune system is not functioning properly, it will not kill the remaining bugs in time and they will reproduce and soon grow to large numbers. Now, when your doctor prescribes some more antibiotics for your infection, they will be useless because all the bacteria are now completely immune to the antibiotic and they will have more time to wreak havoc. So, throw away your "anti-bacterial" soaps, lotions, etc. because there's really that is truly "anti-bacterial" or anti-anything...it's just that more antibiotics are used in these soaps and will kill a larger percentage of the germs on average. This is a sneaky marketing scheme, if you ask me. What you are really doing by buying this stuff is giving these germs a nice environment to mutate in and this will increase the chances of them becoming pathogenic (disease-causing). Normal soap works perfectly well! Thus, the questions are...how do these germs adapt so well (we have some idea), how can we take measures to minimize/prevent multi-drug resistant bacteria in the future and convince doctors to not prescribe them when they are really not needed (and the patients who demand them don't help!), and how can we design better drugs (or should we not at all)? Could nanotechnology (see below) help and should medical doctors be more open-minded to more holistic practices like alternative medicine and energy healing?
Nanotechnology
Crude Analogy: Imagine that you can shrink your computer down to the size of a protein (very small), take it in capsule form, and allow it to carry out functions in your body that you have pre-programmed. Enough said.
This is probably the next revolution in technology (along with quantum computers) where machines are the size of molecules that can be programmed to perform a certain function...the implications are unbelievable for everything from medicine to cosmetics to your own comfort
Adaptive Evolution
Crude Analogy (Ignore terms in parentheses for now and read them later): Imagine that you are one of many chefs (ribosomal subunits) at an outdoor restaurant (ribosome) who receives an order (messenger RNA) and helps makes the dish (protein). However, there is a complication: it seems there is a scary monster (an antibiotic) after you and so you see a black shirt sitting there and decide to put it on (a "random" mutation) so that he won't see you as easily. Well, now the monster won't find you, but you can't cook as fast as before because the shirt absorbs more light from the sun and you get overheated easily. So, there is a tradeoff by wearing the black shirt because even though the monster won't attack you, you can't cook as fast. However, you might be able to do something to compensate for this problem, like say, ripping enough holes in your shirt for air conditioning (compensatory mutations) in order to be able to work at the same speed again. Note that this is a very crude analogy once again - really what would happen would be that another protein like a polymerase (it synthesizes DNA) would alter your DNA sequence, thus causing you to have a black shirt on (the result of a mutation), not really you putting on the shirt yourself, but it's easier to tell the story from the ribosomal protein's point of view.
This concept is essentially the way organisms adapt to their environment through changes in their DNA, but it is much more complicated than this: an example would be that when a certain mutation is made on a bacterial ribosomal (a ribosome is a protein/RNA complex that synthesizes new proteins) gene (a segment of DNA that codes for a certain protein...in the ribosome), the bacteria becomes antibiotic resistant to a certain antibiotic because this antibiotic can no longer bind to the protein...this mutation (call it: ribosomal gene mutation) is costly to the bacteria because now it can not synthesize proteins as effectively as before. To recap, if the ribosomal gene mutation occurs, the bacterial cell is resistant to the antibiotic and now it will live, but there is a tradeoff because now it can not synthesize proteins as well. Which is better and is there a way around it? Yes! So, now let's say the antibiotic is no longer present in the environment...in this case, some of the bacteria in the population revert (this means the mutation is corrected for by going back to its original state) to the wildtype (=no mutation - the ancestral form) and now the bacteria can happily produce proteins again (and since the antibiotic isn't there, it doesn't matter). However, it is more common that there will be compensatory mutations which will compensate for the ribosomal gene mutation - instead of reverting, the mutation is still there in case the antibiotic comes back. To tie it all together, the ribosomal gene mutation is considered a deleterious mutation when there is no antibiotic because it is a cost to the organism, but when the antibiotic is present the mutation is advantageous and would be called an adaptive mutation in this case, so the environment determines what kind of mutation it is. In the end it turns out that these compensatory mutations can resolve the problem of the ribosomal gene mutation so that there's no cost for the bacteria to have that mutation in the first place! Well, it's a bit more complicated than this. All of this makes sense because if all the bacteria in the population (let's say that this mutation is fixed in the population - meaning all of them have the mutation) were to revert and the antibiotic returns (the original environmental state comes back), then they will be in trouble because the antibiotic can now bind. However, if some of them revert and some make compensatory mutations, then the population as a whole will have a better chance of surviving. Now the question is: is this because of random mutations, evolutionary programming for adaptive mutations to occur more frequently than not, complex signaling, quantum evolution, or a combination of any of these?
Adaptive Mutation
Crude Analogy: Imagine the scenario in the "adaptive evolution" analogy, but this time instead of just randomly putting on a black shirt, you just take off your shirt and due to your excessive whiteness, completely blind the monster in the hot sun! In the first case, you didn't know quite what to do, so you just put on a black shirt randomly. In this case, you knew what to do to blind the monster. Taking off your shirt would be equivalent to an entirely advantageous mutation with no tradeoffs (like there was in the black shirt situation). The taking off your shirt situation would be thought of as a "directed" mutation because the mutation was completely directed towards solving the problem with no side effects or tradeoffs, as if you knew what to do. The black shirt situation would be thought of as a "adaptive" mutation because you happened to pick up the black shirt (think of it as a "random" mutation) and it turned out to have adaptive consequences. You might as well have picked up an orange or green shirt to try on because you had no idea that the monster wouldn't see you if you were wearing a black shirt.
So, the term "adaptive mutation" means a mutation that has adaptive consequences, but this is the term now used to describe what was originally called a "directed mutation". This is for good reason because there is considerable evidence that suggests that a cell can not change its DNA sequence to adapt to a *specific* stressful situation. It is thought that any given mutation occurs without respect to its phenotypic (a term used to describe the manifestation of the genotype or entire DNA content of an organism) consequences. In a recent Science paper
Can organisms speed their own evolution? where I will be paraphrasing from.
It recently has been discovered by both the groups of
Susan Rosenberg and
Patricia Foster
that when cells are in starvation conditions (whereby they need to acquire in most cases an adaptive mutation to survive), they can activate the SOS response where certain "error-prone" polymerases are recruited for action. (I say most of the time because it has been shown that cells can survive on eating metabolites secreted from other cells in the population OR adaptively amplifying - expressing a certain gene into a protein - a mutated gene which will give low metabolic activity, but still allow the cells to survive). This SOS response was originally thought to be activated when there was significant DNA damage - such that the normal replicative polymerase could not replicate past the damage. So, it's better to bring in an error-prone polymerase which will be able to replicate past the damage (and make more mutations than the normal polymerase would make) than to not be able to replicate at all because the cell would not be able to reproduce itself with the normal polymerase. OK, now apparently these so-called error-prone polymerases will cause an increase in the mutation rate (hypermutability) in certain regions of the genome (hypermutable hot spots) such that they will increase the chances of having an adaptive mutation appearing. However, it is thought that most mutations are deleterious, so in this case, how does the adaptive mutations thought to be made in this process outweigh the deleterious mutations? That is the main question. It is still not certain what the role of these polymerases actually is because they could be recruited due to the fact that cells in starvation conditions sometimes have more DNA damage than normal. So, it could be a bi-product that happens to increases the chances of survival in stressful conditions. Or there could be less of a cost to turning on the error-prone polymerases, so that's what the cell goes with to conserve energy. It seems that having high mutation rates will help in fluctuating environments, but not in relatively stable environments. Even though cells might be able to turn on high mutation rates at certain times, it might be difficult to turn them off before the deleterious mutations accumulate so high that they outweight the adaptive ones. All in all, it seems that when there are millions of cells undergoing different mutation rates, the ones that acquire an adaptive mutation to an antibiotic, for instance, might not be the cells that have high mutation rates. Natural selection will select the adaptive mutation itself, not the mutator generator (either error-prone polymerases or defects in DNA repair, for example). So, if a cell acquires an adaptive mutation, even though there's a better chance it is from a cell undergoing a high mutation rate, it is as if the mutator generators are "hitchhiking" with the adaptive mutations they produce. Hopefully that makes sense. There are other adaptive strategies to survival in stressful situations, so the important thing to remember is that just because population can't adapt one way doesn't mean it won't evolve another way!
WEIRD SCIENCE
Is there a relationship between music and gene expression?!
Earth Resonance
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