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Amoebas cure cancer atherosclerosis as well as viral diseases
immunotransparent amoebas circulate throughout the body They recognize then eat cancer cytes as well as atherosclerotic plaques The recognize viral surface proteins on tissue removing tissue reservoirs of viral disease curing aids as well as herpes. The amoebas literally attack diseased tissue like a second immune system | |
Amoebas are published as making food choices as a response to their environment
Like human lymphocytes amoebas surround cytes then digest them
Creating amoebas that are immunotransparent to the human immune system permits them to circulate absent immune attack from the body; creating immunotransparency
is a strategy employed with nonhuman mammals thus breeding an immunotransparent amoeba may be literally millions or billions of times easier
Amoebas are publishes as making food choice comparisons; it is possible to make them tissue type specific or possibly even educated to prefer a diseased tissue type specific to a particular person.
The amoebas can be bred or trained to recognize then eat tissue types with particular surface chemistry such as cancer cytes or atherosclerotic lesions. The amoebas literally attack diseased tissue like a second immune system
artherosclerosis as well as cancer were the two most lethal diseases of the 20th century
amoebas that eat cholesterol plaques as well as cancer tissue save billions of lives
Amoebas could be bred or trained to destroy tissue that has active virus surface particles both actively curing viral infections plus removing them from deep tissue reservoirs curing aids as well as herpes.
amoebas may also be injected directly to the core of nonvascular as well as vascular cancers; their ability to reproduce absent oxygen or distant immunogenerative tissues gives them particular strength at removing tumors that lymphocytes cannot reach.
Amoebas are clever enough to choose different foods on purpose
http://www.esajourn...-0358.1?cookieSet=1 [beanangel, Mar 09 2010]
Brain-eating amoeba
http://en.wikipedia...i/Naegleria_fowleri Not this one, i presume (which is actually flagellate) [nineteenthly, Mar 09 2010]
Cancer may just be the cure as soon as we evolve a way to tell it when it has gone far enough.
http://www.ted.com/...re_of_medicine.html [2 fries shy of a happy meal, Mar 10 2010]
now the video with lots of women
http://www.youtube....watch?v=hdzPoHazdnU [beanangel, Mar 13 2010]
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A similar idea to this is mentioned in Larry Niven's 'A Gift From Earth', where a genetically modified rotifer cleans blood vessels. |
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Presumably this would be a marine amoeba used to a tropical environment. I think it would be difficult to avoid a specific immune response. I wonder if it would itself obstruct the circulation, and i think it would probably cause ischaemia at points where the lumina of the blood vessels were smaller than its size. I also suspect there would be disseminated intravascular coagulation. |
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They would also die by a process similar to necrosis. |
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However, i couldn't say any of that for definite, so thanks for making me think. |
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This is an excellent idea apart from a few issues: |
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1) "breeding an immunotransparent amoeba may be
literally millions or billions of times easier [than doing the
same for non-human mammals]" or possibly not. Our
immune system has been working flat out over the last
few hundred million years to try to outwit infectious
amoebae. It hasn't really had to develop strategies for
dealing with an infection of pigs. |
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2) "it is possible to make them tissue type specific or
possibly even educated to prefer a diseased tissue type
specific to a particular person." Possible. Also, "educated"
is a bit of a dodgy concept when it comes to amoebae.
Actually it's a very dodgy concept (even with some
humans). (NB your link didn't work for me for some
reason.) |
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3) What happens if your trained amoebae run out of cancer
cells and still feel peckish? |
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4)-10) another half dozen reasons. |
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But a cute idea nonetheless, and worth thinking on.
Punctuation continues to improve. |
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And then these immuno-transparent amobea mutate slightly, and develop a taste for neural tissue, or muscle, or... |
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And our bodies are completely unable to do anything about it. |
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I do have some respect for this idea, partly because i think small organisms can be seen as tiny machines which could maybe be modified to do something else, rather than building a microscopic machine from scratch. I do think it would be a major undertaking to do so even so, and the question is whether it'd be easier to do this than just making a "nanite". It also breaks an HB tabu: nanotech or genetic modification |
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Molecules can be seen as tiny machines. But once
something becomes self-reproducing, it is by definition
subject to the laws of natural selection, which means it
will evolve solely in such a way as to propagate itself more
effectively. |
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The experience of both conventional breeding and of in-
vitro evolution is usually that the buggers will find a way
to propagate which does not involve them doing what you
thought you were selecting them to do. |
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A truly immune-invisible intracellular organism is only a
point-mutation away from being a really effective
pathogen. |
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Wow, am I seeing semi-colons? |
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No, that's a spot on your lens. |
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What if they could be induced to lose all their nucleic acid somehow? A RBC is pretty simple in some ways (presumably not in others), but it does its job well. What if an amoeba could be induced to function somehow without actually bothering with that whole respiration, DNA transcription/ribosome business? I know it sounds dumb, but if a droplet of dye can be made to negotiate a maze through a pH gradient, could something similar not be done here? |
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I'm thinking tiny organic analogue robots initially organised via DNA which then breaks down. Unfortunately, then a nanomachine really would be more feasible. |
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Then again, there are some organisms which don't seem to mutate very much. |
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I used to be addicted to semicolons, [RayfordSteele]. I had a comma problem and the semicolons moved in to replace them because they lost their force, then colons replaced semicolons and now it's all just a horrible mess. |
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//lose all their nucleic acid somehow?// |
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Now you're talking. You don't even need to eradicate the
DNA, just make sure the buggers cannot reproduce, or at
least can only do so for a defined number of generations. |
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Even without DNA, you can do a lot of things. The only
thing you can't do is to make major changes in gene
expression, and hence you lose some ability to respond to
certain things (but generally in a minutes-to-hours-to-days
way, not a second-to-second way). If the cells retain their
mRNA, they can still to a lot (at least until it degrades),
and there is quite a lot of regulation at the level of the
RNA and beyond. |
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So, this begins to look like a not-quite-so-dumb idea. Just
breed these things (OK, you've still got to make them in
the first place), and then ensure that they can't reproduce
in the body. |
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I'd probably do it by making their reproduction dependent
on at least six synthetic compounds that are not present
in the body. Or, another option, put temperature-
sensitive mutations into several of the genes which are
essential for reproduction (this isn't very difficult to do,
though not much has been done in amoebae). Then breed
the buggers at 25°C. (on the other hand, they might grow
happily in human epidermis, which can often be a lot
colder than body temperature). |
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Basically, you want to cripple them in many ways to avoid
bad things. |
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I would very much like to hear what you all think of this TED talk [link]. |
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Yes, it sounds like that would work really well. Could they maybe be cultured somewhat above body temperature? If it was higher than the highest possible fever, would it not be safe all over the body? Or would that make them a potential tropical form of pemphigus-causing pathogen? |
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The problem is that an organism which thrives at high
temperature will generally survive and reproduce at a lower
temperature, just more slowly. Better the other way
around, I think. |
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Re: High temperature reproduction - every rug burn would become a breeding ground. |
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As I understand it, the main source of evolution is not transcription error mutation, but a combination of jumping genes and expression markers. If you eliminate these, they will evolve much slower (but would still be vulnerable to viral infection, which I think is the biggest threat) |
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If the cell has no ability to create transcriptase, it will not be able to extend its telomeres and so will self destruct after a certain number of generations. |
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//main source of evolution is not transcription error
mutation, but a combination of jumping genes and
expression markers.// |
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Slightly wrong. Evolution arises from mutations in the
DNA, which can arise from various sources. (Evolution is
also driven by recombination between the genomes during
sexual reproduction, if amoebae go in for that). |
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The telomere-lengthening enzyme is telomerase, not
transcriptase. I'm not sure what system amoebae use to
preserve their telomeres but yes, if they use telomerase,
then removing this enzyme would limit their reproductive
ability (unless they mutated around the problem). But
then you'd have to create the amoebae without
telomerase, and you couldn't breed them before injecting
them. |
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[Marklar], in that case anyone who was recently immunised with heat-attenuated organisms had better watch out. |
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[MB], my concern about that is that body temperatures can fall very low in some places, and you only need to look at a Siamese cat to see where those parts of the body would be. |
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Heat-attenuated vaccines are generally "cooked" to kill
them, as I understand it. They don't revive at body
temperatures. |
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Yes, re low body-temperatures. |
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By the time you've finished engineering these creatures to
fit
all your specs, they're not amoebas any more -- they're
lymphocytes with added properties. You might have a
shorter distance to travel if
you started with lymphocytes, rather than amoebas. |
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They could be equidistant from either, [mouseposture]. However, presumably WBCs generally don't become cancerous as WBCs themselves. I could be very wrong and i'm interested in being wrong here, but i'm not aware of a form of leukaemia which arises outside the generating tissues themselves. |
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OK, But I want a to fix the problems in Burma first, is that alright? I'll get right on it afters. |
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Ask a busy person, [WcW]. Or, maybe there's a mysterious link between those problems and not having symbiotic ambæ. |
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if there is then i can't seem to grasp it. I just thought that we should all share our uber-thusiasms for changing the world/destroying all mammalian life. Perspective, yaknow. |
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Maybe this could turn into a biological version of the "grey goo scenario", where all animal life on the planet gets turned into pus. That would presumably be one solution to the problems in Burma. |
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Cancerous white blood cells cause leukaemia, nineteenthly - they are the 'generating tissue'. |
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(white blood cells = leukocytes) |
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Leukocytes' current job is basically what beanangel is proposing. In fact I vaguely remember seeing part of a documentary about research into persuading leukocytes to attack cancerous cells. The problem is really that cancerous cells are hard to distinguish from non-cancerous cells. |
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Yes, but not in the bloodstream or the interstitial fluid, in that as far as i know they don't ever mitose outside the tissues which produce them. That's what i meant. However, i am about to go through the necessary textbooks on this issue. |
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Acute leukaemia: Proliferation in haemopoietic tissues at the expense of other blood components. Can't find a mention of proliferation outside haemopoietic tissues. |
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Acute myeloblastic leukaemia without maturation does have immature WBCs in the bloodstream, but the one with maturation hasn't. What i don't know this second is whether the stem cells are still mitosing at that stage. |
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There's a promyelocytic leukaemia, but again i don't think that mitoses. |
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Need the immunology stuff, i think. |
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If a cell were less differentiated, i suppose the probability of it mitosing outside haemopoietic tissue is higher, so in that way they're like solid tumours. What i'm trying to pin down is what stage they have to get to for mitosis to become impossible, and whether that happens in lymphoproliferative disorders _outside_ the generating tissues themselves. So, either the stage of development the cell reaches once it leaves bone marrow/thymus/spleen/whatever is immature enough for it to mitose while it's out there, or there's a pathological process involving the cells continuing to mitose when they're out there, maybe because they ignore programmed cell death signals or something. |
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Right now, i can't pin it down, but it does confirm me being negative about Echinacea anyway, so it's not a total waste of time for me to do this. |
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Can i have a bit of help here please? |
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Why the video with lots of women [beanangel]? |
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Bottom line: huge number of technical reasons why this
wouldn't work, but it is interesting, and not completely
bonkers. On a very-distantly-related note, the Russians (and
some others) were quite big on using bacteriophage to treat
bacterial infections (OK, very VERY distantly related). |
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There was an old woman who swallowed a fly.. |
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I've solved my own problem, i think. It metastasises
outside lymphoid tissue occasionally at sites distant
from the primary lesion, so there must be WBCs
capable of mitosis in the bloodstream or interstitial
fluid, but it still looks like they're rare. |
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[Nineteenthly] You're asking if leaukaemias produce cells
which continue to divide in the bloodstream? I think
probably yes, a bit, as you indicated. |
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In general, cancer cells mitose like crazy, even if they were
once meant to be terminally differentiated and non-dividing.
But every cancer is actually an ecosystem, and every cancer
is different (I mean every individual cancer, not just every
type). |
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Thanks, yes, i do need to know these things (and i
don't try to treat them, it's so i can give advice or to
help with differential diagnosis). |
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Under normal circumstances, something must stop
them multiplying though. Isn't it possible to use that
somehow (i mean in this idea)? |
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Thought you'd be interested in this one [nineteenthly]. |
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http://newsx.com/story/42685 |
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[nineteenthly] yes, there are many mechanisms which are
supposed to stop cells dividing inappropriately, which is
why it's uncommon for even one of the billions of cells in
the body to break free and become a cancer. I'm not an
expert (though several of my people work on cancers -
mostly lung and colon), but there are all sorts of controls
including contact inhibition and a whole slew of signalling
pathways which either suppress inappropriate growth or
are needed to stimulate normal growth. There are also
cell-death pathways which can kill unwanted or abnormal
cells. |
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Cells become cancerous when they break free of these
controls, and it usually takes several steps for this to
happen. For example, a cell may lose (through mutation)
one gene which normally acts in a pathway to prevent
growth; this may give that cell (and its descendents) a
slight proliferative advantage, leading to local dysplasia (a
patch of odd-looking cells, or a colon polyp, for instance).
Then another mutation in one of that population of cells
may mean that a receptor which normally detects a signal
to trigger replication becomes 'constitutively active' (ie,
it's always "on" even in the absence of the signal), causing
further proliferation. Then cells may lose more growth-
controlling genes (tumour supressor genes), or gain extra
copies of growth-promoting genes (oncogenes), or any of a
variety of other changes. Each change moves the cell
towards greater proliferation, which in turn provides more
opportunities for further mutations to arise. It's basically
a process of natural selection at the cellular level. |
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Finally, a cell acquires the full set of mutations necessary
for unregulated proliferation, for the induction of blood
vessels nearby, and often for metastasis, and then you
are, as medics say, fucked. |
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Most of the new cancer therapies are tailored at the
molecular level, based on an understanding of the
molecular pathways and the ways in which they've gone
wrong. |
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Thanks, [MB], i'm aware of those, but i was thinking
about something more specific - what stops
lymphocytes et caetera from dividing? |
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Ah - sorry. I am fairly confident that I don't know. I guess
(and doubtless you have guessed too) that similar
mechanisms act on normal lymphocytes or their progenitors,
but whether this happens in the haematopoietic tissues or in
the blood or both, I have no idea. |
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Literate blood cells,
Creating a bad haiku.
Haematopoiets! |
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Well, they do get them weird lumpy nuclei. |
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