scientists to look for "evil" gene...

Posted 672 day(s) ago 531 Views 12 Replies
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  1. #1

  2. #2
    OUMallen's Avatar
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    Just a quick inspection of the hair makes me suspicious of Mr. Lanza. Don't need no genealogy.

  3. #3
    but you don't believe in science 87...what gives?

  4. #4
    Originally Posted by greensooner View Post
    but you don't believe in science 87...what gives?
    oh i believe in science...
    but attempting to tie one gene to evil behavior is not science....it's quackery....

  5. #5
    Originally Posted by 87sooner View Post
    oh i believe in science...
    but attempting to tie one gene to evil behavior is not science....it's quackery....
    yeah I'll give you that, it's a reach at best to think that we can target something like that

    likely just an attempt to get money b/c I think the biggest deciding factors on an individual's behavior whether it be good or evil actions are nature/nurture

  6. #6
    beelzeBob's Avatar
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    They have already found it. It is the Y chromosome.
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  7. #7
    Yuck Fu's Avatar
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    Ah so, mutha fucka.

    Originally Posted by 87sooner View Post
    oh i believe in science...
    but attempting to tie one gene to evil behavior is not science....it's quackery....
    Maybe that's not what they are trying to do. Maybe they are trying to identify genetic mutations in this kid that they can compare to others who exhibit similar behavior and see if they can find any consistency.

    Here is an abstract where they are finding mutations that may cause schizophrenia

    Considering the key role of d-serine in N-methyl-d-aspartate receptor-mediated neurotransmission, it is highly relevant to define the role that enzymes play in d-serine synthesis and degradation. In particular, the details of regulation of the d-serine catabolic human enzyme d-amino acid oxidase (hDAAO) are unknown although different lines of evidence have shown it to be involved in schizophrenia susceptibility. Here we investigated the effect of three single nucleotide polymorphisms and known mutations in hDAAO, i.e., D31H, R279A, and G331V. A very low amount of soluble G331V hDAAO is produced in E. coli cells: the recombinant variant enzyme is fully active. Human U87 glioblastoma cells transiently transfected for G331V hDAAO show a low viability, a significant amount of protein aggregates, and augmented apoptosis. The recombinant D31H and R279A hDAAO variants do not show alterations in tertiary and quaternary structures, thermal stability, binding affinity for inhibitors, and the modulator pLG72, whereas the kinetic efficiency and the affinity for d-serine and for FAD were higher than for the wild-type enzyme. While these effects for the substitution at position 31 cannot be structurally explained, the R279A mutation might affect the hDAAO FAD-binding affinity by altering the "structurally ambivalent" peptide V47-L51. In agreement with the observed increased activity, expression of D31H and R279A hDAAO variants in U87 cells produces a higher decrease in cellular d/(d+l) serine ratio than the wild-type counterpart. In vivo, these substitutions could affect cellular d-serine concentration and its release at synapsis and thus might be relevant for schizophrenia susceptibility.
    Copyright © 2012. Published by Elsevier B.V.

  8. #8
    Originally Posted by Yuck Fu View Post
    Maybe that's not what they are trying to do. Maybe they are trying to identify genetic mutations in this kid that they can compare to others who exhibit similar behavior and see if they can find any consistency.

    Here is an abstract where they are finding mutations that may cause schizophrenia

    Considering the key role of d-serine in N-methyl-d-aspartate receptor-mediated neurotransmission, it is highly relevant to define the role that enzymes play in d-serine synthesis and degradation. In particular, the details of regulation of the d-serine catabolic human enzyme d-amino acid oxidase (hDAAO) are unknown although different lines of evidence have shown it to be involved in schizophrenia susceptibility. Here we investigated the effect of three single nucleotide polymorphisms and known mutations in hDAAO, i.e., D31H, R279A, and G331V. A very low amount of soluble G331V hDAAO is produced in E. coli cells: the recombinant variant enzyme is fully active. Human U87 glioblastoma cells transiently transfected for G331V hDAAO show a low viability, a significant amount of protein aggregates, and augmented apoptosis. The recombinant D31H and R279A hDAAO variants do not show alterations in tertiary and quaternary structures, thermal stability, binding affinity for inhibitors, and the modulator pLG72, whereas the kinetic efficiency and the affinity for d-serine and for FAD were higher than for the wild-type enzyme. While these effects for the substitution at position 31 cannot be structurally explained, the R279A mutation might affect the hDAAO FAD-binding affinity by altering the "structurally ambivalent" peptide V47-L51. In agreement with the observed increased activity, expression of D31H and R279A hDAAO variants in U87 cells produces a higher decrease in cellular d/(d+l) serine ratio than the wild-type counterpart. In vivo, these substitutions could affect cellular d-serine concentration and its release at synapsis and thus might be relevant for schizophrenia susceptibility.
    Copyright © 2012. Published by Elsevier B.V.
    Exactly. This is what they did to isolate genetic mutations present in HIV patients that made certain drugs susceptible to specific mutations. By doing so not only were they able to replace and stop treating patients with drugs that have resistant mutations but it also helped them understand the virus better. Heck they also found a mutation(M184V) which if present re-sensitizes the NRTI class of HIV drugs. So as a patient if you have used up that class of drugs, if this mutation comes to the fore later in life it makes you a viable candidate to use them again and prolong your life. Now if you are treatment naive, take your drugs on time and like you're supposed to, you will live a very very long life as a HIV patient.

    But yeah, leave it to 87 to simplify science into calling it quackery.
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  9. #9
    Originally Posted by URNotserious View Post
    Exactly. This is what they did to isolate genetic mutations present in HIV patients that made certain drugs susceptible to specific mutations. By doing so not only were they able to replace and stop treating patients with drugs that have resistant mutations but it also helped them understand the virus better. Heck they also found a mutation(M184V) which if present re-sensitizes the NRTI class of HIV drugs. So as a patient if you have used up that class of drugs, if this mutation comes to the fore later in life it makes you a viable candidate to use them again and prolong your life. Now if you are treatment naive, take your drugs on time and like you're supposed to, you will live a very very long life as a HIV patient.

    But yeah, leave it to 87 to simplify science into calling it quackery.
    i "simplified science" by calling it quackery? is that what i did?

    what did you do when you tried to equate viruses with human behavior?

  10. #10
    Originally Posted by 87sooner View Post
    i "simplified science" by calling it quackery? is that what i did?

    This is what you said:

    but attempting to tie one gene to evil behavior is not science....it's quackery....
    Originally Posted by 87sooner View Post
    what did you do when you tried to equate viruses with human behavior?
    1) No one is equating viruses with human behavior.
    2) The first step towards solving a common problem amongst several different subjects is to find a common cause. Which is exactly what scientists trying to do with evidence and fact based techniques. I know a difficult concept to grasp for you since the paper didnt simply say "God said it so you know, just believe me and have faith. And dont forget to run with it while with clenched fists calling everyone else that doesnt run with you as sinners"

  11. #11
    Originally Posted by URNotserious View Post
    This is what you said:





    1) No one is equating viruses with human behavior.
    2) The first step towards solving a common problem amongst several different subjects is to find a common cause. Which is exactly what scientists trying to do with evidence and fact based techniques. I know a difficult concept to grasp for you since the paper didnt simply say "God said it so you know, just believe me and have faith. And dont forget to run with it while with clenched fists calling everyone else that doesnt run with you as sinners"
    i know exactly what i said.....
    and you dishonestly translated what i said....

    and yes.....you put viruses into the same scientific context as human behavior...

  12. #12
    Just a continuation of a long standing debate between cultural anthropology and cognitive scientists/evolutionary psychology. Anthropologists insist there are actually very few genetically driven behaviors (fear of falling, sex drive, suckling, etc.), but of cognitive scientists, lead most notably by Steven Pinker, are bringing forth serious challenges to those long held beliefs.
    Ashley Montagu would have been one of the older and well known people in the anthropology camp to hold the view than human agression is entirely learned behavior.

  13. #13
    Originally Posted by 87sooner View Post
    i know exactly what i said.....
    and you dishonestly translated what i said....

    and yes.....you put viruses into the same scientific context as human behavior...
    The only commonality between the example cited by me and these scientists is of utilizing common genetic mutations(abnormalities) to better human lives. Thats as far as the similarity goes. But as usual you simplified it, thanks for proving my point.

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