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Cell Death Nets 2002 Nobel Prize in Medicine 116

Posted by timothy from the two-minute-warning dept.
An anonymous reader writes "The recent press release at the Nobel website details the first of the 2002 Nobel Prizes. This year the Medicine prize goes to Sydney Brenner, H. Robert Horvitz, and John E. Sulston for their discovery of programmed cell death (also called apoptosis). Their seminal work in the model organism C. elegans established the foundation of cell suicide as a normal physiologic process. The implications are wide ranging including understanding organ development and cancer."
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Cell Death Nets 2002 Nobel Prize in Medicine More

Cell Death Nets 2002 Nobel Prize in Medicine

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  • Death? (Score:1, Redundant)

    by joyoflinux ( 522023 )
    Probably has some implications in to why we die...could understanding why cells die when they do help create ways to make us live longer?

    • Re:Death? (Score:3, Interesting)

      by Trinition ( 114758 )

      could understanding why cells die when they do help create ways to make us live longer?

      Certainly. For example, there is a theory that free radicals (oxygen atoms sometimes released during the fuel generation accomplished by our mitochondria) cause damage to the DNA of a cell. There are "sweepers" in our cells that are supposed to suck up these free radicals, but som get away and damage our cells.

      Studies have shown in laboratory animals that high-antioxidant diets extend the lifetime of animals. In one particular test, a very simple worm's life was DOUBLED compared ot the control population when a special, synthetic anti-oxidant was fed to it.

      I don't know how related, if at all, programmed cell death is to free radicals and antioxidants, but as you suggested, once you figure out an effect, you can try to figure out a way to prevent or reverse the effect.

      What was it G.I. Joe said? Knowng is half the battle

      • Re:Death? (Score:2, Informative)

        by scrote-ma-hote ( 547370 )
        Yeah, but quiet a few of the studies on humans taking antioxidant samples have had pretty poor results.

        You need to realise that an animal model doesn't necessarily fit with the human one e.g. leptin. Moral of the story: Don't get your hopes up!

        • There's a lecturer I heard once for cancer biology. He started off his lectures with

          "We now can cure every known type of cancer, with minimal side effects to the patient." pause...."In mice."

      • I don't know how related, if at all, programmed cell death is to free radicals and antioxidants, but as you suggested, once you figure out an effect, you can try to figure out a way to prevent or reverse the effect.

        Just don't tell the Vorlons what you're up to. "You are not ready for immortality." - Kosh

    • Re:Death? (Score:5, Informative)

      by sam_handelman ( 519767 ) <samuel.handelmanNO@SPAMgmail.com> on Monday October 07, 2002 @05:31PM (#4406433) Journal
      Yes, but not in the way you think. We can use apoptosis to kill harmful cells, like cancer cells. This is a "natural purpose" of apoptosis, and drugs are under development to "encourage" cancer cells (and virally infected cells) to die by this mechanism.

      The theory that apoptosis plays a central role in human aging is part-and-parcel of the "free radical" theory of aging, which I think is bullshit.

      The basic idea is that reactive oxygen species - these are chemicals that want to take electrons away from biological molecules and can do in such a fashion that the biological molecule is damaged - damage your mitochondria [utmb.edu] in such a fashion that the mitochondria signal the cell to die. This definitely CAN happen - however, I don't believe that it actually does, or that any of the pathologies we observe in human aging actually depend on this pathway. Btw, I'm a bioinformatician (grad student); when I worked with my Dad, I studied oxidative stress - he still does but he does not think it plays a role in normal aging. Certain conditions - being a chain smoker, being on hemodialysis, whatever - may actually put enough of these reactive oxygen species into your system that this could happen, but I doubt it.

      FYI: some people try to sell you antioxidant dietary supplements (or other treatments.) I cannot emphasise enough - these products are snake oil. Even if reactive oxygen species do play a significant role in aging (which I doubt,) taking spills to scavenge them or soak them up is utter malarky.

      The opinion of someone with whom I disagree almost completely. [web-books.com] More of the same - the summary is fairly accesible. [ufl.edu]

      To sum up - I can't say conclusively that there is no aging-related process that depends on apoptosis, but I don't find the evidence at all convincing. The one that people are fond of at the moment, which is oxidative stress-come-apoptosis, is hogwash.

      Aptoptosis serves two functions:
      1) Developmental. Developmental Aptoptosis is necesarry to "carve out" your body. For example, when your fingers form, the tissue between what will become the fingers goes aptoptotic and dies. There is no real evidence that this is what happens when you get old.

      2) Defensive. Cells which are pre-cancerous, or which have been infected with viruses, can become apoptotic. Certain conditions that some old people get - autoimmune disorders, for example - depend on apoptosis to do harm. However, this is not a part of normal aging.

      P.S. Most scientists pronounce it "apo-tosis," [celldeath-apoptosis.org] the p is silent (like pterodactyl.) On the other hand, by this reasoning, helicopter (which comes from the same root as pterodactyl) would be "heli-coter", so say the p if you want.
      • Good post.

        I like to pronounce it a-pop-tosis because it really helps to imagine the cell going *pop*. :)
        Yay mnemonics!
        • Most people pronounce it that way, but it's wrong. It's actually pronounced "ape-oh-toe-sis". The second p is silent and both o's are long.

      • Whaaa? (Score:3, Funny)

        by spun ( 1352 )
        Someone posted a link to an opinion opposing his own on slashdot? This is SLASHDOT! We don't tell both sides of the story here, my good man.
      • Uhh, AFAIK, the programmed cell death = why we age theory has nothing do do with the various free radical charlatans.

        Rather, programmed cell death in the context of aging has to do with the loss of telomeric DNA, (non-coding 'tags' on the end of DNA molecules that form a place for DNA polymerase to bind when copying the DNA).

        The part of the telomere where the DNA poly first binds doesn't get copied & eventually (after reaching a number of divisions known as the 'Hayflick limit') the cell has no more telomeres & so can't divide anymore, at which point it undergoes programmed cell death.

        There are other signals that activate PGD, such as viral infections and early stages of cancer (where the sad association with vitamen C overdosing came in: if the cell was damaged by 'free radicals', it should undergo apoptosis, but this would be a symptom not a cause), but the type of PGD usually referred to in aging studies is this 'molecular clock' that keeps count of how many times the cell has divided in aging (of some tissues) is then caused by many cells of that tissue reaching the hayflick limit and self destructing.

        This theory of aging doesn't seem to completely cover the issue, but it does have alot more backing in scientific research than the free radical stuff. More:
        http://www.nature.com/nsu/020819/020819-13. html

        Interestingly, many "Lower" animals, along with germ (sperm & egg progenitors) cells & cancer cells make an enzyme called telomerase which rebuilds the telomere, making these cells essentially immortal.

        On the subject of aging, Geron is trying to find ways to reverse some effects of aging (at least those caused by PCD due to shortened telomeres) using telomerase:
        http://www.geron.com/02.01_telomerase .html
        • I agree, apoptosis and necrosis due to oxidation are not the same thing, but if you agree with the current elucidated mechanisms, they are not unrelated.

          The point that they have in common is alteration of mitochondrial membrane permeability. In apoptosis, different signal transduction cascades (initiated by factors such as FasL found on cytotoxic T cells that can therefore kill virus-infected or tumor cells, TNF [tumor necrosis factor] secreted by macrophages in inflammation, and tumor suppresor genes like p53 and Rb which initiate apoptosis after sensing DNA damage) affect the balance between pro-apoptotic proteins (e.g. Bax and Bad) and anti-apoptotic proteins (e.g. Bcl-2 and Bcl-XL). (These proteins are analogs of the ced gene products found in C. elegans) If the pro-apoptotic proteins win out, mitochondrial membrane permeability is altered, cytochrome c gets dumped into the cytosol (essentially stopping ATP production), and the caspases (which are also proteins that are analogs of the ced gene products) are activated and proceed to effectively dismantle the cell. Similarly, oxidation of the cell membrane alters cell permeability, causing, among other things, a massive influx of calcium, which in turn also alters mitochondrial membrane permeability, once again dumping cytochrome c into the cytosol and activating caspases.

          Another way that oxidation is linked to apoptosis is that free radicals damage DNA. The damaged DNA is sensed by products of tumor suppressor genes such as p53 and Rb, and apoptosis is initiated.

          In most cases of pathological cell death, both necrosis (which is essentially the unregulated death of a cell due to loss of membrane integrity, inadvertant release of destructive enzymes, and destruction of critical regulatory proteins) and apoptosis (which is by contrast exquisitely regulated) are occurring simultaneously.

          And while telomerase serves an interesting purpose in regulating the cell cycle, it is by no means the only cause of aging. Most of the pathology of aging is caused by mechanical and structural damage to cells: the accumulation of intracellular debris, wear and tear on the cytoskeleton, damage to the genome. While free radicals aren't the only factors that cause this damage, they undoubtedly do have a significant effect.

          Telomerase is only important in cells that continue to divide, but the organ systems that are most affected by aging are typically populated by cells that don't really reproduce at all or at least reproduce very infrequently, such as neurons in the brain and myocytes in the heart.
          • > but the organ systems that are most affected by aging are typically populated by cells that don't really reproduce at all or at least reproduce very infrequently, such as neurons in the brain and myocytes in the heart.

            Well, certainly most folks who die of old age (as opposed to infection or cancer) lose either their mind or their heart, yes. But reduced function in which cell types in these organs is the cause (rather than the symptom)? The clogging of neurons in the brain (alzheimer's) eventually gets is all, but that's not _caused_ by reduced function in the large neurons, right?. & on the other hand, while the number of large neurons doesn't increase, there are many neural cells that continually divide.
            http://courses.umassmed.edu/mbb1/CNS_over view/Cell ularAnatomy.cfm

            As for myocytes, aren't most of the aging related diseases of the myocytes due to reduced or absent blood flow to the myocytes? & isn't this blood conducted by endothelial cells, which like skin cells, reproduce a great deal during a person's life?

            I think if you think about it, most of the aging related things folks die of (in the context of cells simply wearing out rather than some active dis-ease) can be related to reduced function in the rapidly reproducing tissues, esp. endothelial & epithelial tissues.
      • How then do you explain so-called reperfusion injury, which is definitely a real phenomenon on the gross level? Current molecular explanations revolve around either the idea that once apoptosis is initiated, it is irreversible, or the idea that the restoration of blood flow and hence oxygen supply actually adds fuel to the flames by creating even more free radicals AKA reactive oxygen species. Most likely, it is some combination of both, and even though control of apoptosis will not completely stop such injuries, it could at least reduce it and thereby change the outcomes of patients who have strokes or heart attacks.
      • I have always pronounced it with the "p" silent. I don't know why, but hearing people pronounce the "p" irritates the crap out of me.....
    • Another way you can avoid dying is to avoid stepping out in front of that bus.
    • i'm delighted that Dr. Horvitz has garnerd this prize. My only question is why did not the Nobel Committee discover my paper written as a first-year medical student in which i proposed that there exists just such a mechanism for cell death, mediated by a DNAse enzyme. For this I was awarded a summer cancer research fellowship, in 1980.

      Oh well, my debts probably exceed the value of the prize, making the impact of such a prize so minimal on my earthly existence. ;)

      jon anderson, md
      tkjtkj@charter.net

  • Dead cells _can_ come back... (Score:5, Funny)

    by PissingInTheWind ( 573929 ) on Monday October 07, 2002 @05:05PM (#4406288)
    by eating the yummy, healthy brain of a living.

    See here [theonion.com].

    Mmmm... braaaaiiinnnss...
  • programmed cell death With the new technamolagical advances in biology, i wonder if it would be possible to "reprogram" these cells to have an infinite life span.
    • i wonder if it would be possible to "reprogram" these cells to have an infinite life span.

      Sure. It happens naturally.

      Usually, we call it cancer.

      • Sure. It happens naturally. Usually, we call it cancer.

        So, at the cellular level, what is it that makes us age?

        • Re:ever living cells (Score:4, Insightful)

          by Daniel Dvorkin ( 106857 ) on Monday October 07, 2002 @05:38PM (#4406477) Homepage Journal
          If you can answer that question, you'll be getting the next Nobel Prize in Medicine or Physiology. "What makes us age?" is one of those deceptively simple questions in biology, like "How do proteins fold?" that seems like it should be simple to answer but turns out to be fractal in its complexity -- the closer you look, the more details emerge, and the closer you look at those details ... etc.
      • Isn't cancer caused by cells multiplying too rapidly? Is an issue of exponential growth, where they just keep multiplying and old ones don't die off? If we could make periodic adjustments to the way cells replicate perhaps this would work? I assume that at some point all the cells start slowing down the split process. If we could periodically change that point to equalize between cancer and failure, might we live longer?

        I've also heard that hair/nails can still grow for some time after death? I suppose those cells keep on going. Creepy

        • Re:Cells not dying or over-multiplying? (Score:2, Informative)

          by Anonymous Coward
          It is both. The cell would stop reproducing and die if it were working properly. It _may_ also reproduce at an accelerated rate or detach and float around in the blood stream.

          But the main problem is that it and it's "children" won't die. If they did, the problem would fix itself (due to the limited number of times the cell can divide plus the limited lifetime).

        • Re:Cells not dying or over-multiplying? (Score:4, Interesting)

          by Idarubicin ( 579475 ) on Monday October 07, 2002 @07:33PM (#4407147) Journal
          Isn't cancer caused by cells multiplying too rapidly?

          It's a little bit of both. Cancer is the result of uncontrolled cellular replication due to genetic damage to cellular regulatory machinery. Apoptosis is supposed to kill off cells that have problems with their internal structure (for example, a genetic error causing a fault in the systems that regulate growth and proliferation) as well as cells at the end of their useful lifespan.

          If we could make periodic adjustments to the way cells replicate perhaps this would work?

          And you've just hit on the holy grail of oncology. Unfortunately, we can't just tell all the body's cells to commit suicide. Cures cancer--but results in unsatisfied customers. And some quickly replicating cells are supposed to be that way (bone marrow, gut lining, hair, etc.) so we can't even just mow down fast-growing cells. Actually, that's sort of what chemo and radiation therapies do in a very ham-fisted way--toast all the fast-growing cells, and hope that the cancer dies faster than the rest of the body. It's why chemo makes your hair fall out, and causes anemia and nausea.

          Rest assured, however, that your tax dollars are hard at work on a solution.

          I've also heard that hair/nails can still grow for some time after death? I suppose those cells keep on going. Creepy

          This one is mostly an urban legend. Mostly, it's due to the slight dessication/dehydration the body underdoes after death. There's a bit of evaporation, and shrinkage. Contraction of surrounding tissue can force hair and nails to protrude further than before death, giving a perception of growth. Also, there were cases up until the last century or so that involved patients in deep coma states--still alive, but apparently dead. Yes, hair and nails grew on those 'dead' people. And they got pissed off when they got buried.

          • that the key to the immortality that we seek possibly lies in the cancers that plague us?

            Cancer is just a bunch of immortal cells. (ie: won't undergoe apoptosis)

            Reminds me of the Hela Virus cells that were collected from Henrietta Lacks still sitting in some fridge somewhere...

    • Yea, they call it cancer. (Score:1, Informative)

      by Anonymous Coward
      There are a number of issues in going from making a cell live forever, and making us do so.

      First, you have to develop. Wouldn't want to make a 6 year old's cells live forever.

      Then, you have to repair. You need to balance growth with externally induced damage (injury, sickness). If you make cells live forever, you also have to stop them from dividing... Or you'd end up quite the mess.

      Many cells in the body, like skin, grow and die and that is very important to us. If the didn't die, you'd slowly erode the dead surface and end up one quivering blob of ozing red pain.

      • So life is based on certain cells being able to die and be replaced, and others lasting somewhat of a longer time. Is the problem that the long-living cells eventually die off, or that other cells stop/slow their multiplication process or both.

        I suppose in the cases of people who don't die of outside caused, death would generally be caused by heart failure? Interestingly enough, I've not heard of tumours growing in hearts, or of people having dying of heart cancer, but perhaps it happens and I just haven't heard of it. The heart would probably be a good place to start though, trying to keep it from degenerating too much in later years.

        In an additional note, it might be noted that many of the creatures that live the longest are also not overly prolific. If we were to mess with our genes so we lived longer, we might disable the human ability as far as bearing many offspring.
    • There are such things as immortal cells [nature.com]. You can make [yale.edu] them in a lab.

  • To nitpick a bit (Score:5, Insightful)

    by Otter ( 3800 ) on Monday October 07, 2002 @05:07PM (#4406303) Journal
    ...Sydney Brenner, H. Robert Horvitz, and John E. Sulston for their discovery of programmed cell death (also called apoptosis).

    To be precise, the Horvitz lab at MIT discovered apoptosis. Brenner and Sulston were honored for their roles in establishing C. elegans as an experimental system.

    Why study a nematode, you ask? They're small, transparent (so they don't need to be dissected) and are self-fertilizing. Most interestingly, they have a precise number of cells that arise from an entirely predictable series of divisions and deaths, making it easy to pick out genes that affect that process.

    • To nitpick a bit (more) (Score:1, Informative)

      by Anonymous Coward
      "To be precise, the Horvitz lab at MIT discovered apoptosis. Brenner and Sulston were honored for their roles in establishing C. elegans as an experimental system."

      I believe Horvitz actually conducted the seminal work (first discovering and characterizing genes controlling cell death) while working (along with Sulston & Brenner) as a postdoc at the MRC (in the UK).
      • Yeah, as I was writing the bit about cell lineage I realized that they must have recognized that they were dealing with predictable cell death.

        I think we're converging on the correct timeline, which was that the cell lineage work was done at the MRC, in large part by Horvitz, but the identification of genes did happen at Horvitz's own lab at MIT.

        Anyway, the initial point was that, whoever did what where, Horvitz is primarily associated with apoptosis while the other two are known for generally developing the whole C. elegans system.

    • Uh, no. Sulston and Horvitz observed apoptosis while working together at the MRC lab i Cambridge, UK. I know this because I have a book in prf about the worm, and have talked at length to both men about the process. Sulston was the first man to see it happening. Horvitz' lab later isolated the genes involved.

  • Quick link/explanation (Score:5, Informative)

    by perrin5 ( 38802 ) on Monday October 07, 2002 @05:09PM (#4406312) Homepage
    NPR has a pretty good link [npr.org] to an explanation. At the top of the article, there's an real audio recording [npr.org] of the actual report that I listened to this morning. I thought it was fairly accurate, and should give some explanations.

    To be precise about it, these fellows did not "discover" apoptosis, they have done a lot of very good work defining the genes and methods responsible for triggering it. From what I've read, though, they certainly deserve the prize.

  • Cell death (Score:5, Funny)

    by silvaran ( 214334 ) on Monday October 07, 2002 @05:15PM (#4406341)
    I didn't know people were dying from using cellular phones... No, not that kind of cell death.

  • kill them off BEFORE they commit suicide (Score:5, Funny)

    by michaeljmuller ( 260771 ) on Monday October 07, 2002 @05:19PM (#4406359)

    i think it's inhumane to let your cells get to the point where they have to commit suicice. i euthanize my weak cells with jack daniels on a periodic basis.

  • Nano-Suicide Booths (Score:2, Funny)

    by Anonymous Coward
    Please select mode of death:

    1. Quick and painless
    2. Slow and painful
    3. It doesn't matter, you're genetically predisposed to die a horrible, horrible death. (Sorry, no refunds)

  • To the Nobel Institute: (Score:1, Funny)

    by Anonymous Coward
    This is to notify you that I have contacted the office of Attorney General John Ashcroft to legally prevent the ritualistic suicide of these countless cells. He, as a True Christian (tm), will not stand for these wicked acts.

  • As an american (Score:2, Offtopic)

    by Chundra ( 189402 )
    I must urge the free people of the world to root out these cells, and prevent their evil ways from spoiling our way of life. We must support a preemptive strike! We must initiate a regime change! How many more Americans must die because of these suicidal cells. It's biological terrorism and we must put a stop to it, or watch our children suffer.

  • A practical example (Score:2, Interesting)

    by madcoder47 ( 541409 )
    After working for several years at an Immunology lab at Harvard, It's very nice to see people finally get credit for discovering apoptosis. I use it in the lab as a core immunosuppressive therapy, only in mice and monkeys as of yet -- and by harnessing the power of apoptosis (PCD) we have so far created a treatment which acts like a powerful immunosuppressant to transplanted allografcts, without all the harmful side effects.
    .
    While it may sound pretty violent or harmful, Apoptosis is not only a natural process, but it has also opened up new gateways into research in many different fields.

  • Understanding Cell Death and Regulatory Switches (Score:5, Interesting)

    by Salis ( 52373 ) on Monday October 07, 2002 @05:43PM (#4406504) Journal
    The next step is to quantify the signals (chemicals) responsible for triggering the series of events that are called apoptosis and to elucidate just how transcription switches work. All 'switches' in the body are based off the concentration of various molecules, be they enzymes, cofactors, structural proteins, minerals (Na+, K+, Ca+), etc. The most interesting exploration would entail studying how a concentration of a signal yields a binary switch, that an event either be triggered or not.

    The cell widely uses feedback loops, both positive and negative, to exponentially increase and decrease the amount of signal that is being produced at any one time. This signal may interact with other signal-producers to give a multi-signal, multi-enzyme response system that, through the non-linear dynamics of the system, yields a definitive high and low concentration of signal that determines whether an event is to be triggered or not.

    To fully understand the mind-boggling complexity of a single cell, imagine a system composed of 5000 enzymes (or more) all interacting with 10,000 molecules (or more) with thousands of possible reactions. Now try to simulate this all at the same time, using non-linear kinetics, and predict the outcome of an initial state.

    A lot of crazy things happen, including shifts in entire groups of genes (responsible for protein & sRNA synthesis) caused by very tiny disturbances. The non-linear dynamics of the cell are set up so perfectly that its self-regulation is simply amazing.

    My Two Cents...not meant to be a full explanation of why apoptosis is so cool or where the research is going from there.

    Salis
  • When I heard this announced I kept confusing these guys with UCSF's Dr. Cynthia Kenyon [ucsf.edu], who was on Scientific American Frontiers [pbs.org] not long ago talking about her work with elegans and their age-resistant genes. Anyone know what's the difference between her research and these guy's?
  • Evolutionary psychology has pointed out that it is possible for suicide to be evolutionarily advantageous. If my existance makes it less likely that my genes will be replicated, then it would be evolutionarily advantageous for me to kill myself.

    For example, if I am a large drain on my family, and I'll never be able to have children, and I'll just make it harder for my siblings to get by, then my existence will make it harder for my (siblings) genes to be replicated.

    Of course, this is almost never actually the case. But it makes sense that perhaps it used to be, when we didn't have such a easy time surviving. Now those same urges, that may have made sense when most people died by the time they were 30, are completely out of place.

    Same basic concept.
    • I would agree with your point that under some circumstances suicide can enhance inclusive genetic fitness, however not all behaviors are genetically programmed, and this possibility does not in itself constitute evidence that suicide is the result of a genetic predisposition. Higher thought processes are often just emergent properties of complex interactions between simple components, rather than direct expressions of genetic information. Thus there are often behaviors that have no genetic purpose but are merely an outgrowth of other behaviors that do serve a purpose. Suicidal behaviors may or may not have been evolutionarily selected for, but could just be a part of the price we pay for other traits that are advantageous. More importantly though, your point is not really relevant to the topic. Cell suicide is not really relevant the suicide of an organism. Cell suicide is one tool which our body uses to direct growth and development of the body as a whole. It is a necessary part of life, not something that only happens to end a life.
      • Right. I exactly do not mean that there are genetic traits leading to suicide. I just mean that sometimes it is advantageous to die. Same for an individual cell as for a whole person. Individual cells have many more (and more codified) reasons.

        And, aside from the metaphor:

        You say, "Suicidal behaviors may or may not have been evolutionarily selected for, but could just be a part of the price we pay for other traits that are advantageous." I completely agree. That's exactly what I mean. I'm trying to suggest that one of the advantageous behaviors that lead modern humans to commit suicide might have been suicidal in the first place. Now, since our environment/society has changed faster than our genetics, those tendencies are engaged in all kinds of incorrect situations.

        Also, I'm not trying to take credit for the idea. I hope I haven't totally misrepresented the proponents of evolutionary psychology.


        • Ever seen an injured snake or wild mouse? They do not try to run and hide, but turn belly up (more visible). Are they commiting suicide before predators to protect offspring?

          Perhaps it's just playing possum.

          No animals were harmed in the posting of this comment. PETA (People Eating Tasty Animals) oversaw it's production.
          • Sometimes animals will freeze so that predators will not be able to see them. Sometimes they will play dead so that their potential predators will think they have been dead a long time and will not be good to eat.

            Neither of those really fit the situation I'm talking about. I definitely can't think of an animal that does anything like it. It's a hypothesis, not a proven theory.
    • Like anything Evolutionary (Sociology, Politics etc etc) arena except Biology there is one uniting factor in the application of Evolution theory to another area. It doesn't make sense, and is founded on the standard lack of understanding of science found throughout the fluffy subjects, as Rutherford said

      "All research in the social sciences can be summed up by the phrase 'some do, some don't'.

      To mention on the same page as Noble Prize winners a bunch of mumbo-jumbo just shows what an unscientific world we live in.
      • Well, fair 'nuff.

        I should point out that it was in a psych course on personality theory that I was briefly exposed to the subject of evolutionary psychology. Even the guest lecturers who discussed it were totally up front about the lack of experimental data on the subject.

        It's just a valuable way of looking at people. Not more valuable than many others. ydig?
  • Back in first grade, they teased him when he would play with worms during recess. He swore he'd show them, and now...

    Millions of seven-year-olds were inspired today to poke at slugs and other slimy invertebrates.

  • Unrelated to human death. (Score:5, Informative)

    by madcoder47 ( 541409 ) <<ten.redocdam> <ta> <tnempoleved>> on Monday October 07, 2002 @05:47PM (#4406531) Homepage Journal
    Programmed cell death is a natural cellular process (as natural as cellular respiration, for that matter)

    It is vital to development of many tissues, such as nervous tissue in the spinal cord or the brain. Death of a human is not massive PCD.

    Programmed cell death / apoptosis is caused by intercellular communication.

    Apoptosis can be stimulated in a cell through a variety of ways, for example in an antigen-presenting immunoreactive T-Cell which binds through a Fas / FasLigand compliment, the t cell will undergo apoptosis and kill itself so that it cant kill the other cell.

    So in reality, no, it has nothing to do with human death, just regular cell death.

    • In english (Score:3, Informative)

      by Shook ( 75517 )
      In the example he gave:

      Say a cell is infected by a virus, it will present pieces of the virus on the cell surface.

      A T-Cell comes along, checks out this virus piece, and sends a signal saying
      "Hey, that's a virus! You're infected! It would be better for all of us if you just commit suicide."

      After getting this signal, the infected cell turns on its apoptosis genes and kills itself in a sensible, precisely controlled manner.

      This is just one example of apoptosis, but you can see how the controlled suicide of a few cells is beneficial to an organism.
    • So when all your cells die, you go on living?

      If so, we've found the scientific foundation for defining the afterlife.

      Seriously, some cell death is vital for correct development of the tissues and complex structures that we all carry around. But by understanding cellular death, we might better understand cellular stasis and cellular growth. Every piece of the puzzle hints at what is missing.

      • It's not all your cells dying, which is the only reason you are wrong.

        Different cells have different cell-surface receptors. Some receptors create apoptotic signals within the cell, others don't. It is a direct result of external happenings within your body... i.e. a T-Cell binds to a cell with a nonself antigen which also expresses Fas Ligand. Only THAT cell will die.

        Not massive cell death, death of certain targeted cells bearing certain apoptotic receptors.
  • The big question in programmed cell death research is how does one pronounce apoptosis. Is it literally a-POP-tosis or is the second p silent, as if we were ancient greeks? I thank the Academy for the honour but the debate will still rage I fear.

  • Sorry abut the raw-HTML post above. I forgot to switch from code mode. Here is the correct version:
    Because it is an interesting and often misunderstood subject, here is a small primer on the topic of apoptosis (Programmed Cell Death).
    FYI I work in an immuno lab which uses apoptosis as a main treatment for transplant tolerance.

    Death by suicide

    Cells that are induced to commit suicide:

    • shrink
    • have their mitochondria break down with the release of cytochrome c
    • develop bubble-like blebs on their surface
    • have the chromatin (DNA and protein) in their nucleus degraded
    • break into small, membrane-wrapped, fragments
    • The phospholipid phosphatidylserine, which is normally hidden within the plasma membrane is exposed on the surface.
    • This is bound by receptors on phagocytic cells like and dendritic cells which then engulf the cell fragments.
    • The phagocytic cells secrete cytokines that inhibit inflammation.

    The pattern of events in death by suicide is so orderly that the process is often called programmed cell death or PCD. The cellular machinery of programmed cell death turns out to be as intrinsic to the cell as, say, mitosis.

    Why should a cell commit suicide?

    There are two different reasons.

    1. Programmed cell death is as needed for proper development as mitosis is.

    Examples:

    • The resorption of the tadpole tail at the time of its metamorphosis into a frog occurs by apoptosis.
    • The formation of the fingers and toes of the fetus requires the removal, by apoptosis, of the tissue between them.
    • The sloughing off of the inner lining of the uterus (the endometrium) at the start of menstruation occurs by apoptosis.
    • The formation of the proper connections (synapses) between neurons in the brain requires that surplus cells be eliminated by apoptosis

    2. Programmed cell death is needed to destroy cells that represent a threat to the integrity of the organism.

    Examples:

    Cells infected with viruses One of the methods by which cytotoxic T lymphocytes (CTLs) kill virus-infected cells is by inducing apoptosis. (And some viruses mount countermeasures to thwart it.) Cells with DNA damage Damage to its genome can cause a cell
    • to disrupt proper embryonic development leading to birth defects
    • to become cancerous.

    Cells respond to DNA damage by increasing their production of p53. p53 is a potent causer of apoptosis. Is it any wonder that mutations in the p53 gene, producing a defective protein, are so often found in cancer cells (that represent a lethal threat to the organism if permitted to live)?

    Cancer cells Radiation and chemicals used in cancer therapy induce apoptosis in some types of cancer cells.
    • Wouldn't we be able to eliminate cancer then by assuring the p53 gene is properly producing proteins? Or any variation of this... Wouldn't we be able to destroy every dangerous cell by killing anything that has a mutated p53 gene? Is there a part of cancer research devoted to this p53 topic?
      • The problem with p53 is that cancer cells contain a mutated p53 gene.

        Normal nonmutated p53 acts as a tumor suppressor, binding to genomic DNA and starting gene expression of p21 if the DNA copy is incorrect (as is the case with cancerous cells with genomic mutations) .

        p21 halts the cell division, stopping reproduction of the cancerous cell.

        In a already cancerous existing cell with a p53 mutation, the cell will divide normally, because the p53 is mutated and it cannot bind DNA effectively. Therefore, the p21 will not get signalled, and the cancer will continue to multiply.

  • Apoptosis 101 (Score:3, Interesting)

    by DjMd ( 541962 ) on Monday October 07, 2002 @06:08PM (#4406654) Journal
    People have asked and speculated as to the usefullness as to preventing or inducing apoptosis.

    Cancer is caused by mutation on a single cell level. In order to divide, grow, resist the immune system, spread locally, develop a blood supply, and finally spread to distant sites a cell needs to mutate.

    The list of mutations literally reads as check list of to-do's... Some of the first level requirements involve turning on the growth cycle, and turning off the mechanism of automatic cell death. Many cancers are 'immortal' cells. It is litterally one cell that grows and divides. Cloning itself over and over...

    If you could force the cells to apoptose, (or disable their overide of the natural apoptotic cycle) you could defeat a great many cancers...

    That is of course an over simplification, most cancers do the same thing but the method they use is very different (thus there is no magic bullet on the horizon)


    How do I know? check the name djmd

  • Another kind of cell death (Score:3, Funny)

    by r_j_prahad ( 309298 ) <r_j_prahad@NOSpAM.hotmail.com> on Monday October 07, 2002 @06:21PM (#4406735)
    Cell phone.
    Humongous gas guzzling SUV.
    Inattentive soccer mom.
    Unlighted bicycle on same roadway.

    That's what came to mind skimming the headline, cell phone death. I gotta sell my bike, it's making me paranoid.
    • Cell phone: $99
      Humongous gas guzzling SUV: $32,000
      Inattentive soccer mom: free (god knows there's enough of them)
      Bicycle on same roadway: $199
      Video sent in to Real TV showing gruesome death: priceless.
  • Both Sulston and Dr. Robert Waterston (of Washington University in St. Louis' Genome Sequencing Center [wustl.edu]) later went on to pioneer the sequencing project for the C. elegans genome, completed in 1998 (Notes on the project, as written in Science [wustl.edu]).

    I'm half-expecting Waterston to also get the Nobel sometime in the near future, once the entire public human genomic sequencing effort has yielded all of its results. The processes and data gained have been valuable to the entire community to a whole, and he's been instrumental in bringing everything together.

  • Cell death?

    What prize do I get if I kill a cat in the name of quantum physics?
  • Damn you, Cytochrome C!!!

    I'll get you...you and your little friends BAX and BCL-XL, too!

  • This is rather interesting because a couple of weeks ago I was discussing with some friends how Brenner got cheated out of a Nobel for his work in discovering apoptosis -- so finally he gets one. I guess he just had to live long enough for the idea to become trendy.

  • Ok (Score:2)

    by Raul654 ( 453029 )
    Am I the only one whose first thought was that it was referring to deaths caused by cell phones?
    • Am I the only one whose first thought was that it was referring to deaths caused by cell phones?

      Step 1: Someone develops a way to host a web site from a 3G phone.

      Step 2: A story about the phone gets posted on Slashdot

      Step 3: ...

  • "...Sydney Brenner, H. Robert Horvitz, and John E. Sulston for their discovery of programmed cell death (also called apoptosis). To be precise, the Horvitz lab at MIT discovered apoptosis. Brenner and Sulston were honored for their roles in establishing C. elegans as an experimental system." From what i know on the subject matter(I will discuss later), apoptosis was not discovered by Horvitz's lab, but was discovered in what i believe was the early 70s by Kerr, Wyllie, and Curie, three British doctors. I am not positive on the dates, or their actual specialities, but I do know for a fact that those three were the first to discover the phenomenon known as apoptosis. I know this all because despite me being only a high school student, I spent the last two years working on my Intel Science Research topic in the field of apoptosis. Unfortunately I never found a mentor and was dropped from the program, but I do have a very good understanding of the process as I would attend monthly meetings at MSKCC in NYC for an attempt to better understand.Email me if you wish to flame me or whatever.
  • Maybe they can explain to my why my Cingular phone cuts out in the middle of my F*ING CALLS!
  • Is "Sex and the Origins of Death [amazon.com]." by William Clark. Well written, easy to read. He introduces cell death and describes necrosis as well as apoptosis. Discusses some of the ideas behind what apoptosis means (propagation of the species versus propagation of the individual) for organisms. Towards the end, goes into some possible applications for longer-life, etc. Good Book.
  • 'Bout damn time. After so many episodes of Goku, Gohan, Vegeta, and Piccolo powering up, all interrupted by flashbacks of past seasons and the original series, I didn't think they'd ever get around to Cell's Death.

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