i don't think they would film anything before the person died either way.
planet earth took years and years to film. i'm not suggesting this will be anywhere near as good as planet earth, just that production companies have plenty of time on their hands. it's not like someone is going to scoop them.
i would argue that psychology provides descriptive explanations because biology has yet to reach the sophistication needed to chemically explain the disorders.
i reject the notion that humans will never be explainable. at the moment, the human brain seems to me to be completely out of our intellectual and technological grasp... that's why I didn't major in neuroscience and picked genetics instead. but it's simply a matter of time.
i don't believe that it is completely negative. one of my favorite authors is oliver sacks, who has taught me a lot about the myriad amazing abilities people with autism (and for that matter, other 'disorders') have.
i do think that it's a little tough to call something an 'autistic' trait though. autistics can display enhanced abilities compared to 'normals,' but as far as I know there aren't many things that are completely unique to those with autism. it's a matter of degree. might be semantics though.
those with such abilities (that we can recognize anyway) are on the higher-functioning end of autism. those autistics with less communication abilities are often very hard on their families, and i find it hard to believe that they would have even survived back in cave days.
i don't think there should be a systematic effort to eradicate autism. there should be more options available to us to understand and perhaps improve the lives of those with severe autism.
i completely understand the community of people who see it as just another 'style' of humanity, rather than a deficit. you can see the same attitudes in the blind and deaf communities. but having seen some families turned on their heads by an autistic child, I also understand the desire to find better treatments/'cures.'
i agree. in this way, I see autism as similar to schizophrenia. not in symptoms, but in the sense that there are likely thousands (millions?) of possible genotypes that lead to what we have come to call autism. they are also similar in the sense that there is tremendous range to the severity of symptoms.
i do believe that we will be able to reduce the incidence of both in the future. through a combination of genetic counseling, IVF with selection for high-risk parents, and drugs taken during pregnancy. pure speculation at this point though.
"Whether it's cemented at "birth" is beside the point of this drug as it attempts to correct a current state not prevent one. They claim it works on adult animals they have tested. RTFA? Nah this is/. lets just make assumptions."
looks like we're going to have to do a close reading here, for the sake of your education.
In your first clause of your first sentence, you directly refer to my comment about the possibility that autism may be "cemented at birth," (meaning that regardless of which small molecules you give to someone with autism caused by fragile X syndrome, there will be no effect). You therefore made it clear that you were also talking about autism caused by fragile X, and not simply fragile X itself. In your second clause (where your main misunderstanding of the facts/developmental biology seems to lie), you state that there is a distinction between 'correcting a current state' and 'preventing one.' The main mistake you are making here is connecting the mGluR5 receptor with autism. This connection appears nowhere in the article, and is likely the result of you reading too fast. Your second sentence continues with this incorrect idea. You correctly point out that the mGluR5 inhibitors appear to have reduced some non-autistic symptoms in adult mice. However, because your original statement was about autism, not fragile X (because my statement was about autism, not fragile X generally, and you were responding to me), you committed a logical mistake.
i'll state it again, just for you. there is no evidence that the seizures and protein synthesis abnormalities seen in animal models of fragile X are causationally related to autism. a small fraction of autism cases in people appear to be linked to a gene that is upstream of the mGluR5 receptor, but that definitely doesn't mean that the drugs that antagonize the receptor will have any effect on autism. again, even if this receptor does play a role in autism, it could be at a specific developmental stage, making the drugs useless for treating the disease in people. that is what i meant by "cemented at birth."
and you did extrapolate. let's detail it for you. you made the assumption that because these mGluR5 antagonists reduced some neurological symptoms in animal models, that autism would be similarly affected. granted, you never said this explicitly (perhaps you were too busy insulting me?). the context of your comment makes it crystal clear though. by responding to my post about autism, you made your comment about autism too. and you mistakenly said that the drugs mentioned in the article, "attempts [sic] to correct a current state not prevent one." In the context of autism, this is not true in the least.
feel free to keep it coming though. me and my degree in molecular and cell biology have all night.
the article is about a drug that targets a rare genetic trait. because the article appears in layman media and is remotely linked to autism, the submitter titled the/. story "Startup Tests Drugs Aimed at Autism," which is only mildly true.
My original comment:
"i sure hope autism isn't something that is more-or-less cemented at birth, making drugs like these not very useful."
i was tacitly talking about the minority of autism cases linked to this fragile X syndrome, as evidenced by the fact that I was talking about "drugs like these." I was trying to make the point that, even though the drug has been shown to mitigate some of the symptoms of fragile X in adult animals, this tells us nothing about whether the drug will have an effect on autism. i.e. autism's link to fragile X could be completely unrelated to the symptoms of fragile X seen in the animal models (seizures, abnormal protein synthesis, etc). We have no idea what all the functions of FMRP are. anyone who says we do is a fool.
it is entirely possible that mGluR5 has nothing to do with autism. it could simply be a receptor in a downstream pathway from FMRP, separate from whatever pathway(s) are involved with autism development. furthermore (getting back to my first post), even if this receptor is somehow involved with autism, it could be involved only at a very specific stage in development. thus, giving mGluR5 antagonists to people who have passed that stage would have no effect.
thus your comment:
"Whether it's cemented at "birth" is beside the point of this drug as it attempts to correct a current state not prevent one. They claim it works on adult animals they have tested."
is practically worthless, even without the rude bit at the end that I left out. they have only shown that some non-autism symptoms of fragile X are mitigated in adult mice. it's poor form to extrapolate as you seem to be doing when there is no evidence to support it. might i recommend a biochemistry course?
i sincerely hope these drugs do work. but even if they do it will only affect ~5% of the population of people with autism.
lol. people on here can be such punks sometimes...
i probably should have elaborated my point. what I meant was that it is entirely possible that autism is the result of a developmental process that occurs before birth. the animal models you mention are not of autism itself, but of fragile X syndrome. TFA says that the syndrome is associated with less than 5% of autism.
the key point is, "While it's not yet clear if there is a critical window during development for giving the drug, adult animals still benefit from the treatment." There is no evidence yet that this will translate to any effect on autism, even in those with fragile X.
so before you mouth off next time, RTFA yourself.
true, but still leaves the problem of brain drain. what do you we do about the immediate issue of spending resources on people and not recouping them except in long-term political/social ways.
this has little to do with the alleged crimes. if anything, they indicate to me that the guy wasn't really that bad. have you seen the kinds of things on those low schedules?
regardless, this has to do with a company handing over personal information without the laws that govern that company saying they had to. ergo, bowing down.
“I did a search off the IPaddress to locate him,” said Roberson. “I got a longitude and latitude. Then I went to Google Earth. It works wonders. It uses longitude and latitude. Boom! I had an address. I was not able to go streetside at the location, but I had him.”
this doesn't seem accurate. ip address -> long/lat -> address? no chance. i can believe that they used his ip to find him, but probably through his ISP. In my experience, those geographic traces are only very rough estimates. sounds like this cop thinks he lives in CSI or something. i wonder if any of it is true?
that's what i'm trying to get at. unless the neural link confers an advantage to the survival of the animal in the wild, there's no way it would persist. one of darwin's most beautiful insights was that no trait in nature exists solely for the enjoyment of humans (except of course in humans). my further point was that the level of complexity of such a link would lead one to believe that if the ability to bond with humans is in fact a detriment to the overall fitness of an animal (not just health, but ability to spread one's germ line widely among the wild population), then it should be able to evolve to prevent the connection with humans. the complexity should allow a specialization where the wild animals retain the use of the link for their own intraspecies uses, and block the genetically negative or neutral connection with people.
the neural connection would have to be much much more complicated (and thus less permutable) than what is involved with ducks bonding to people.
we're getting pretty deep down the rabbit hole with this one, but I remember during the movie that one a wild animal was 'bonded,' it seemed to leave its native community and become domesticed, ie removed from the wild gene pool. sure, they could have gone back out to the wild from time to time to 'intermingle,' but what's the selective pressure to maintain the ability to get domesticated among all of the wild population?
Slashdot Mirror
i don't think they would film anything before the person died either way.
planet earth took years and years to film. i'm not suggesting this will be anywhere near as good as planet earth, just that production companies have plenty of time on their hands. it's not like someone is going to scoop them.
i wasn't suggesting it should be someone youngish. i just think it would remove some of the morbidity it they didn't use the word terminal.
Why does the person need to be terminally ill? why can't it just be someone who agrees to be mummified following their death?
are the producers that impatient?
yeah... you're right.
this is why I'm a bio major.
bingo. it's flux (change in magnetic field), not the magnetic field itself, that produces a current.
i would argue that psychology provides descriptive explanations because biology has yet to reach the sophistication needed to chemically explain the disorders.
i reject the notion that humans will never be explainable. at the moment, the human brain seems to me to be completely out of our intellectual and technological grasp... that's why I didn't major in neuroscience and picked genetics instead. but it's simply a matter of time.
i don't believe that it is completely negative. one of my favorite authors is oliver sacks, who has taught me a lot about the myriad amazing abilities people with autism (and for that matter, other 'disorders') have.
i do think that it's a little tough to call something an 'autistic' trait though. autistics can display enhanced abilities compared to 'normals,' but as far as I know there aren't many things that are completely unique to those with autism. it's a matter of degree. might be semantics though.
those with such abilities (that we can recognize anyway) are on the higher-functioning end of autism. those autistics with less communication abilities are often very hard on their families, and i find it hard to believe that they would have even survived back in cave days.
i don't think there should be a systematic effort to eradicate autism. there should be more options available to us to understand and perhaps improve the lives of those with severe autism.
i completely understand the community of people who see it as just another 'style' of humanity, rather than a deficit. you can see the same attitudes in the blind and deaf communities. but having seen some families turned on their heads by an autistic child, I also understand the desire to find better treatments/'cures.'
i agree. in this way, I see autism as similar to schizophrenia. not in symptoms, but in the sense that there are likely thousands (millions?) of possible genotypes that lead to what we have come to call autism. they are also similar in the sense that there is tremendous range to the severity of symptoms. i do believe that we will be able to reduce the incidence of both in the future. through a combination of genetic counseling, IVF with selection for high-risk parents, and drugs taken during pregnancy. pure speculation at this point though.
"Whether it's cemented at "birth" is beside the point of this drug as it attempts to correct a current state not prevent one. They claim it works on adult animals they have tested. RTFA? Nah this is /. lets just make assumptions."
looks like we're going to have to do a close reading here, for the sake of your education.
In your first clause of your first sentence, you directly refer to my comment about the possibility that autism may be "cemented at birth," (meaning that regardless of which small molecules you give to someone with autism caused by fragile X syndrome, there will be no effect). You therefore made it clear that you were also talking about autism caused by fragile X, and not simply fragile X itself.
In your second clause (where your main misunderstanding of the facts/developmental biology seems to lie), you state that there is a distinction between 'correcting a current state' and 'preventing one.' The main mistake you are making here is connecting the mGluR5 receptor with autism. This connection appears nowhere in the article, and is likely the result of you reading too fast. Your second sentence continues with this incorrect idea. You correctly point out that the mGluR5 inhibitors appear to have reduced some non-autistic symptoms in adult mice. However, because your original statement was about autism, not fragile X (because my statement was about autism, not fragile X generally, and you were responding to me), you committed a logical mistake.
i'll state it again, just for you. there is no evidence that the seizures and protein synthesis abnormalities seen in animal models of fragile X are causationally related to autism. a small fraction of autism cases in people appear to be linked to a gene that is upstream of the mGluR5 receptor, but that definitely doesn't mean that the drugs that antagonize the receptor will have any effect on autism. again, even if this receptor does play a role in autism, it could be at a specific developmental stage, making the drugs useless for treating the disease in people. that is what i meant by "cemented at birth."
and you did extrapolate. let's detail it for you. you made the assumption that because these mGluR5 antagonists reduced some neurological symptoms in animal models, that autism would be similarly affected. granted, you never said this explicitly (perhaps you were too busy insulting me?). the context of your comment makes it crystal clear though. by responding to my post about autism, you made your comment about autism too. and you mistakenly said that the drugs mentioned in the article, "attempts [sic] to correct a current state not prevent one." In the context of autism, this is not true in the least.
feel free to keep it coming though. me and my degree in molecular and cell biology have all night.
here we go, buddy:
/. story "Startup Tests Drugs Aimed at Autism," which is only mildly true.
the article is about a drug that targets a rare genetic trait. because the article appears in layman media and is remotely linked to autism, the submitter titled the
My original comment:
"i sure hope autism isn't something that is more-or-less cemented at birth, making drugs like these not very useful."
i was tacitly talking about the minority of autism cases linked to this fragile X syndrome, as evidenced by the fact that I was talking about "drugs like these." I was trying to make the point that, even though the drug has been shown to mitigate some of the symptoms of fragile X in adult animals, this tells us nothing about whether the drug will have an effect on autism. i.e. autism's link to fragile X could be completely unrelated to the symptoms of fragile X seen in the animal models (seizures, abnormal protein synthesis, etc). We have no idea what all the functions of FMRP are. anyone who says we do is a fool.
it is entirely possible that mGluR5 has nothing to do with autism. it could simply be a receptor in a downstream pathway from FMRP, separate from whatever pathway(s) are involved with autism development. furthermore (getting back to my first post), even if this receptor is somehow involved with autism, it could be involved only at a very specific stage in development. thus, giving mGluR5 antagonists to people who have passed that stage would have no effect.
thus your comment:
"Whether it's cemented at "birth" is beside the point of this drug as it attempts to correct a current state not prevent one. They claim it works on adult animals they have tested."
is practically worthless, even without the rude bit at the end that I left out. they have only shown that some non-autism symptoms of fragile X are mitigated in adult mice. it's poor form to extrapolate as you seem to be doing when there is no evidence to support it. might i recommend a biochemistry course?
i sincerely hope these drugs do work. but even if they do it will only affect ~5% of the population of people with autism.
what if what you think is red is actually blue to me lol!
lol. people on here can be such punks sometimes...
i probably should have elaborated my point. what I meant was that it is entirely possible that autism is the result of a developmental process that occurs before birth. the animal models you mention are not of autism itself, but of fragile X syndrome. TFA says that the syndrome is associated with less than 5% of autism.
the key point is, "While it's not yet clear if there is a critical window during development for giving the drug, adult animals still benefit from the treatment." There is no evidence yet that this will translate to any effect on autism, even in those with fragile X.
so before you mouth off next time, RTFA yourself.
yawn. is this supposed to be sarcasm? wrong forum, buddy. don't feed the trolls kids. it's what they want you to do.
i sure hope autism isn't something that is more-or-less cemented at birth, making drugs like these not very useful.
one of my favorite papers ever: Apples and Oranges: A Comparison
true, but still leaves the problem of brain drain. what do you we do about the immediate issue of spending resources on people and not recouping them except in long-term political/social ways.
given the less-than-open nature of.... well, everything in china, it isn't as simple as that.
they found an old copy of revelations a while ago that said 616, not 666 is the number of the beast.
this has little to do with the alleged crimes. if anything, they indicate to me that the guy wasn't really that bad. have you seen the kinds of things on those low schedules?
regardless, this has to do with a company handing over personal information without the laws that govern that company saying they had to. ergo, bowing down.
you'd think they'd want a subpoena to cover their own butts in the event that the cops got it wrong and the guy sues them.
“I did a search off the IPaddress to locate him,” said Roberson. “I got a longitude and latitude. Then I went to Google Earth. It works wonders. It uses longitude and latitude. Boom! I had an address. I was not able to go streetside at the location, but I had him.”
this doesn't seem accurate. ip address -> long/lat -> address? no chance. i can believe that they used his ip to find him, but probably through his ISP. In my experience, those geographic traces are only very rough estimates. sounds like this cop thinks he lives in CSI or something. i wonder if any of it is true?
that's definitely not true at all. you just want people to get egg on their trousers. wow, i've never used the word trousers before.
robot hand + machine-written journalism = infinite fun!
that's what i'm trying to get at. unless the neural link confers an advantage to the survival of the animal in the wild, there's no way it would persist. one of darwin's most beautiful insights was that no trait in nature exists solely for the enjoyment of humans (except of course in humans). my further point was that the level of complexity of such a link would lead one to believe that if the ability to bond with humans is in fact a detriment to the overall fitness of an animal (not just health, but ability to spread one's germ line widely among the wild population), then it should be able to evolve to prevent the connection with humans. the complexity should allow a specialization where the wild animals retain the use of the link for their own intraspecies uses, and block the genetically negative or neutral connection with people.
the neural connection would have to be much much more complicated (and thus less permutable) than what is involved with ducks bonding to people.
we're getting pretty deep down the rabbit hole with this one, but I remember during the movie that one a wild animal was 'bonded,' it seemed to leave its native community and become domesticed, ie removed from the wild gene pool. sure, they could have gone back out to the wild from time to time to 'intermingle,' but what's the selective pressure to maintain the ability to get domesticated among all of the wild population?