GDG

My understanding is that a defibrillator works by delivering a large enough charge that all of the heart muscle cells are depolarized, and thus unable to contract until they have restored their ion imbalances. Basically, it takes all the overactive muscle cells and gives them a "time out." This interrupts the fibrillation (if successful). I'm not sure how transplanted hearts are restarted, but I suspect they use a temporary pacemaker. This also shocks the heart, but at a much smaller voltage, and in an appropriate rhythm. The idea here is not to depolarize all the cardiac tissue, but rather to stimulate the heart's natural pacemaker to begin initiating contractions.

I'm not sure the odds are quite that low, as genes are not inherited completely independently, but mainly in large groups (aka chromosomes). Yes, there is some exchange of genes between different homologous chromosomes (and unfortunately I cannot find any data for the frequency of that happening in humans). However, even if you start with identical twin fathers marrying identical twin mothers, the odds that their children will inherit the same assortment of 22 chromosomes is infinitesimal. For that matter, consecutive children of the same parents have the same odds, but you hardly ever hear about identical twins being born several years apart

The As and Ts are on complementary strands, as are the Cs and Gs. In double stranded DNA, you would have a structure like (for example) this: ATGGCGATTAC ||||||||||| TACCGCTAATG One strand is the "sense" strand, and the other is the complementary strand (although both strands can encode proteins). The DNA is transcribed into mRNA (which looks just like DNA, except that you have the base "U" (uracil) instead of T, and have one more hydroxy group on the sugar part of the molecule). When the mRNA is translated to protein, the enzymes that do the transcribing (a complex called a ribosome) reads the bases three at a time: each group of three is called a "codon", and each codon codes for a specific amino acid (or for "stop"). ATG GCG ATT ACC ||| ||| ||| ||| TAC CGC TAA TGG (Note: I'm only putting in the spaces to identify codons -- the ribosome does not physically separate the bases.)

According to this , they need no modification at all.

I think you're thinking of Evolutionary Computation and genetic algorithms. The second concept there is the "Singularity", first posited by Vernor Vinge. The idea is that once we (a) succeed in creating artificial intelligence, and (b) manage to make the AI smarter than humans, the AIs will rapidly make themselves more and more intelligent, at an exponentially increasing rate, until they've left us far behind. The state of the world afterwards is literally unimaginable. Despite being unimaginable, it has become a popular trope for science fiction authors. Ray Kurzweil is probably the author most known for writing seriously about the singularity.

p [math]\propto[/math] N where p is the probability the geometric object was made by humans, and N is the number of human footprints in the vicinity. For crop circles, p = 1.

There are extreme disorders in which half the brain fails to develop, or must be surgically removed early in childhood. Even with half a brain, the person generally is able to do everything an intact human can. This sometimes requires extra training and time, but the brain is capable of shifting functions around. However, this is not to say that there is no difference... Again, I have to recommend "The Brain That Changes Itself" by Norman Doidge for anyone interested in this kind of stuff. Phineas Gage is often cited as the first example of a lobotomy. IIRC, he was pretty bad-tempered before the accident, and much ... calmer afterwards. This was the inspiration for the neurosurgical procedure (pre-frontal lobotomy), which could be performed by inserting a long needle upwards through the eye socket, severing the connections betwen the prefrontal lobes and the rest of the brain with a few swipes. Unfortunately, those doctors failed to follow up on Gage's later life: he was utterly unable to make plans, handle money, etc., and died a very unhappy man.

Julian B. Barbour seems to think so. See his book "The End of Time". You can read a big chunk of it on Google Books. Personally, I don't think the case is made very convincingly.

Epilepsy is "excessive, abnormal, or synchronous" brain activity. This does not mean that constant and widespread activity is excessive or abnormal. The point is that many people think that parts of your brain just sit there and do nothing. This is untrue: you do not have 95% of your brain lying fallow and available for other purposes (e.g., like backing up your memory, as if the brain were a hard drive with damaged sectors). While it is true that structures in the brain like the hypothalamus, basal nuclei, hippocampus, etc., probably cannot be repurposed, large parts of the cortex are subject to pretty rapid reassignment. If you go blind tomorrow and start learning braile, a chunk of your visual cortex will end up reassigned to interpreting the patterns you detect with your index finger. All of it gets used.

Unfortunately, that is completely contrary to Relativity. Not that Relativity is unassailable, but you'll have to show where the equations are wrong before anyone will take this seriously.

They do indeed add up, but you have to consider each force as a vector (not just magnitude, but also direction). Some forces may (partially or fully) cancel each other out.

First off, it is not true that the brain uses only a small percentage of its capacity. This is a common misconception, probably arising from a misunderstanding of the work done by Wilder Penfield. WP was the brain surgeon who famously stimulated parts of the cerebral cortex while operating on patients with epilepsy: the patients then reported what they experienced. The idea behind this was to cut out the spot that was causing seisures while avoiding cutting out any tissue that was "important". For example, if stimulating a particular spot caused the patient's index finger to move, WP figured that that spot of brain controlled the finger, and that removing that spot would effectively paralyze the finger (so he didn't remove such spots). Over time and numerous patients, WP developed a map of the cortex with locations for various body parts (sensory and motor), hearing, language, etc. Most of the spots, however, had no obvious function. The key word there is "obvious." The fact that WP could not determine what the function was does not mean that the spot had no function. Later experiments have shown that some of these spots have pretty subtle functions, like the ability to identify nouns, or adjectives, or recognize animals, or power tools. Obviously, when you have a patient lying in the operating room with their skull open, you cannot test for absolutely every possible function. It is much more likely that absolutely every part of your brain is used, particularly as it is known that neurons that are not used are subject to apoptosis -- literally "use it or lose it." At present, the only sort of human tissue that we can keep alive indefinitely is essentially tumor tissue. Doesn't make for very good brains Assuming that the medical problems are worked out, however, there would be no need to resort to "brains in jars". The brain is a tissue, just like the rest of the body: if you can arest aging in the brain, you should also be able to do so throughout the rest of the body -- with much more comfortable results

Actually, you are not the first person to think of this. For example, it was a fad in Japan in the 1920's, but was shown to be without any scientific basis. The idea was also popular with the Nazi's...

Well, your brain does control many aspects of your body and its functioning that you are never aware of. For example, your digestive system does not run by itself: your brain and spinal cord regulate all of the secretion, peristalsis, etc., even though you have no conscious control over the process. What I think is most likely in the situations that you are talking about is that the person in question is determined to survive until event X (grandchild's birth, or wedding, or birthday Y, etc.), and after that point, relaxes. I.e., it is not so much the force of will keeping the person breathing when they "should have" already passed on, as it is the terminal patient who is satisfied that they've made their milestone "letting go" after it is done.

In question #1, if blood cell production was greater than blood cell destruction, you would have an ever-increasing number of blood cells. Eventually, your blood vessels would be packed solid -- not good. Conversely, if production was less than destruction, you would have an ever-decreasing number -- anemia. Also not good. I think a) through d) are correct: unfortunately, you can't say that e) is not true... Question #2 -- correct. Question #3 -- you haven't given an answer. However, I think you'll find the answer here if you look.

Yes, viruses need enzymes: typically, their genomes encode only one or two structural proteins (and even these may also have an enzymatic activity), and everything else is an enzyme of some sort. Common types are polymerases (to replicate the viral genome), proteases (some viruses express their genome as one long "poly-protein", which is then cut into individual proteins: typically, the protease is at the end, and first cleaves itself from the rest of the polyprotein), and enzymes that modulate the cell's defenses. Viruses are so stripped-down that inhibiting any of its enzymes usually helps. (The exception is proteins like HIV's nef (IIRC), which keeps virus replication suppressed most of the time.) Generally, just inhibiting the enzyme is sufficient, without also attaching the "magic bullet." Targetted liposomes have been tried for things like delivering chemotherapeutics to cancer cells, or antifungals to pathogenic fungi. It is difficult to target to a cell infected with a virus, because for the most part it looks like any healthy cell. If everything is operating properly, the infected cell will cleave some of the viral proteins and present the resulting peptides on its surface, bound to the cell's MHC proteins. This, of course, is why successful viruses inhibit MHC expression. The real problem with cytotoxic liposomes, though, is selectivity. Nothing is 100%. Even if you had an antibody that was really, really specific for the target cell, some of the liposomes are going to stick, non-specifically, to innocent bystanders. Blam, they're dead. The reason this is tolerated in cancer treatment and combatting fungal infections is that the diseases are so serious that collateral damage is acceptable. Wouldn't do to give the patient chemo-like side effects when treating the flu. The idea of administering compounds that inhibit the viral enzymes is good, though. This is the approach that most pharma companies use when developing antiviral drugs. It still isn't simple, though, as the compound still has to make it into the cells without being metabolized, and without unduly interacting with any of the patient's thousands of other enzymes. At least most small molecule drugs are small enough that the patient does not develop antibodies against them (although this can still happen if the drug happens to bind to a human protein, like serum albumin).

What is most clear is that we do not completely understand the immune system yet. See for example: G. Pacheco-Lopez et al., FASEB J (2009) 23(4):1161-67, which describes how to train rats so that their conditioned response to the taste of saccharin is a depression in immune response; A. Kusnecov et al., Biol Psych (1989) 28:25-39, reviewing research regarding immunomodulation by behavioral conditioning; J. Kipnis et al., Proc Natl Acad Sci (2004) 101:8180–85, describing how depletion of T-cells degrades cognition (and restoring T-cells restores cognition) Given those unexpected findings (at least to me), I would hesitate to say that the immune system has clear limits and capabilities...

Check out Music Therapy, for starters...

If you really think you are communicating by telepathy, perhaps you should check out the Rhine Research Center. Otherwise, "sharing the same soul" is more of a poetic concept than a scientific idea. The "soul", pretty much by definition, is something that cannot be weighed, measured, or otherwise detected. How can we say you two have the same soul, if we can't extract it, pin it to a board, and identify its distinguishing characteristics? Since these are the Science Forums, you're not likely to get the answer you're looking for here. Personally, I think you're both just infected with the same memes, from close contact and native susceptibility.

Unfortunately, this is a little more complicated than it sounds. Suppose you have identified the human receptor that the virus uses to gain entry into the cell. It is sometimes possible to clone the receptor and truncate the part that binds it to the membrane (this does not work for all receptors), and make what is called a "soluble" receptor. ("Soluble" because you have eliminated the hydrophobic anchor that would otherwise keep it bound to the cell membrane.) I think this is basically what you are proposing. The first problem is that by truncating the protein, one often disturbs the structure of the receptor protein. It may be a subtle change, but often this is enough to change the binding affinity for the virus by a factor of 10 (or more). Of course, it is also possible that the binding would increase (but this is less likely). So the decoy protein will still bind the virus, but you'll need a higher concentration in order to shift the equilibrium away from binding the native receptor. OK, let's assume that you've solved the first problem, and can make decoy protein that binds the virus just as well as the native form of the receptor. The second problem is that the decoy protein is now unfamiliar to your body, and you will develop an immune response to it. Just by truncating the end, you expose a part of the protein that was previously inaccessible to the immune system, which will treat it as foreign. Sometimes this can spill over into an immune reaction against the native receptor, in which case you have a nasty autoimmune problem (e.g., myasthenia gravis), the symptoms of which may be disabling or deadly, depending on the receptor and the strength of the response. OK, let's assume you've solved the first two problems. Perhaps you got lucky, and there is already a native soluble receptor (there are such things, although I have not heard of one serving as a viral entry). You still have the problem (#3) of flooding the body with something which binds not only the virus, but whatever the receptor's natural ligand is. If that ligand is important, you may not have improved the patient's health. Suppose the target receptor binds insulin: by administering a lot of insulin receptor decoy proteins, you might mop up all of the patient's insulin along with the virus, thus giving the patient immediate iatrogenic diabetes. Sure, you can modify the decoy so that it no longer binds to the natural ligand, but then you are back at problem #2, with a foreign protein. OK, let's assume that you've managed to solve or ignore problems 1-3: the final problem is that protein drugs tend to be more expensive than the regular chemical type (what we call "small molecules"). The economics of health insurance basically dictate that this drug would be used only for really serious/lethal infections. Actually, let's go back and check one of our assumptions: not all receptors can be truncated (let's call this problem #0). Some receptors are integrally a part of the cell membrane (e.g., 7TM-GPCRs, 7-transmembrane G-protein-coupled receptors, which cross the cell membrane 7 times), and cannot be truncated without completely falling apart. Having said all that, sometimes you will find a receptor that you can work with, and develop a drug that may be immunogenic, but would not have to be administered for long enough that it would be cleared out by your immune system. If you're lucky, disrupting homeostasis by mopping up some of the natural ligand doesn't unduly perturb the patient. And perhaps the disease is lethal enough, or terrifying enough, that patients will pay for it. Your final problem is mutation. All pathogens mutate at some rate (retroviruses tend to be the fastest). If your new drug stops all of the viruses that have the "original sequence", you will find that some small fraction of the viruses have already mutated such that either (a) they now bind to the original receptor better than your decoy (this can happen if your decoy is not identical to the original receptor), or (b) they now bind a related but different receptor (your body is full of receptors that resemble each other structurally). Start over

Sounds like Gatorade...

Again, Wikipedia has a pretty good entry.

Schrodinger's cat is a fine thought experiment, but we can't take it too literally. Quantum states decohere rapidly if exposed to the environment. Certainly, the colony is not going to be in a superposition of states because (a) it interacts constantly with its environment, and (b) there are way too many observers. And I'm not sure that the original Schrodinger's cat setup would remain in a superposition of states for a substantial length of time.

Wikipedia has a pretty good entry on this. Interestingly, some photocopies have this feature too (or at least, they used to). Try using a light blue pencil on text: when you photocopy it, the blue pencil should not show at all. Sometimes works with blue highlighters too.

For the degree of relationship, one looks to homologies between various genes. You can derive a numeric score that says how closely related two organisms are. Fungi cell walls contain chitin, the same stuff that is found in insect exoskeletons and crustaceans.