But prions don't actually reproduce--they already exist in our brains. All mammals have prion proteins in their brain. The propagation starts when one of these normally folded one misfolds, or a misfolded one gets into the brain from some other source. Then it causes the existing proteins to misfold. No new molecules are created in this process. In fact, a disease form of a prion is the exact same molecule as a healthy form. It's just a change in shape. Viruses don't hit on all the hallmarks of life, and prions hit even fewer.
Remember: We all have proteins that can act like prions. The prion protein responsible for mad cow disease is in the brains of all cows, and a version is in all people. It's a misfolded form of the protein that causes disease.
And most people with prion diseases don't get it from eating meat. Only about 1% of prion diseases come from infections--eating animal meat with misfolded prions, for example. Up to 20% of people with diseases have genetic mutations that cause the misfolding. But about 80% of the cases are just sporadic misfolding of unknown cause.
Also prion diseases are super rare--about 1 case in a million people. So prions in meat is a pretty low risk situation.
What this study is showing is that classical prion proteins aren't the only ones that misfold and then get other proteins to misfold with them, causing disease in the process. Basically, what this group is saying is that "prion" is a much broader concept in biology--that many proteins beyond the mad cow ones can act like that.
Right now there are no drugs that stop or even slow Alzheimer's or Parkinson's. And that's not for a lack of trying. There have been several notable failures recently--drugs that went to clinical trials and showed no effects in patients. These drugs were designed before this idea that all these diseases were due to prionlike mechanisms started to pick up steam in the field. So now that there have been some fairly big papers suggesting that prionlike proteins are the cause, people can start looking at new designs for drugs that would stop prionlike propagation. Basically, people have already been doing that for classical prion diseases--making molecules that stop those proteins from aggregating into fibrils. So now drug makers could take all that's been learned with those molecules and apply them to Alzheimer's and Parkinson's.
Usually the compound in your pill is not the compound someone fished out of a microbe. It's been modified to give it better pharmacological properties--last longer in your bloodstream--and to avoid toxicity issues. So there is a lot of intellectual work that goes into making the compound you ingest even if the initial inspiration came from a fungus.
No one takes a molecule from a bacterium or fungus and then starts giving it to patients. You have to find the specific compound that allows the fungus/bacterium to kill its neighbors--a very labor intensive process. Then you have to get its structure. Then you test it to see if is druggable--will it last long enough in the bloodstream to be effective, for example. It probably isn't, so then you need to synthesize analogs and test them. Then you have to test it for toxicity, maybe synthesize more analogs to get around toxicity problems. And then you can start clinical trials--three rounds of them usually. Somewhere along the way you need to devise a way to make the compound in large enough quantities to turn it into a pill or injection or whatever deliverable form you're picking.
So there are a lot of steps between "hey this compound from this fungus killed that bacteria," and "take this pill once a day for 10 days."
The use of the term reflects the usage by materials scientists. The titles of both papers describe the materials as 2-D. It is an established term in the field.
"a material in which the atomic organization and bond strength along two-dimensions are similar and much stronger than along a third dimension"
REF: http://pubs.acs.org/doi/full/1....
Materials scientists use "two-dimensional" to describe graphene and similar materials. These are materials that consist of essentially a single molecular/atomic layer.
Really? How do they know it wasn't just raw sewage, or industrial chemicals if they didn't even identify the chemical, or even prove it came from the oil spill?
The PNAS paper that looked at the SF Bay spill ruled out sewage and other chemicals found in the Bay. They suggest sunlight transformed crude compounds into toxic ones. The PNAS paper is in front of a paywall, I believe: http://www.pnas.org/content/109/2/E51.full
Its not that the oil is "missed", its just that the oil once degraded to the point that it is not oil anymore is hard for them to measure with current methods, so they can't figure out where it went.
The main point, is that the oil is gone, degraded, oxidized, etc. The most dangerous (to marine life) part of the spill is gone.
But where degraded oil goes is a question scientists want to know, mainly because they don't fully understand what those compounds do to wild life. So even if the chemicals aren't the ones that originally spilled into the ocean, what they become is still of interest to researchers, because they know less about them.
They haven't identified specific compounds yet--sounds like that is next on their to-do list. The scientists definitely think the compounds arise after the oil spills out of the well and sits out in the sun for a bit. Basically you're right: They're talking about the end results of oil degradation. But the big question is what do these chemicals do to marine life. Are they toxic? Or do they just sit around and living things ignore them.
They make the nanoparticles from silane gas. The process is very energy intensive and produces CO2. So a pretty long tailpipe on this technology. You probably need more energy than you can create. Also it's unclear if these particles are better than magnesium hydride, which is the material of choice in many prototype fuel cells.
Slashdot Mirror
Here is a story from Science that reports some skepticism in the conclusions: http://news.sciencemag.org/hea....
But prions don't actually reproduce--they already exist in our brains. All mammals have prion proteins in their brain. The propagation starts when one of these normally folded one misfolds, or a misfolded one gets into the brain from some other source. Then it causes the existing proteins to misfold. No new molecules are created in this process. In fact, a disease form of a prion is the exact same molecule as a healthy form. It's just a change in shape. Viruses don't hit on all the hallmarks of life, and prions hit even fewer.
Remember: We all have proteins that can act like prions. The prion protein responsible for mad cow disease is in the brains of all cows, and a version is in all people. It's a misfolded form of the protein that causes disease. And most people with prion diseases don't get it from eating meat. Only about 1% of prion diseases come from infections--eating animal meat with misfolded prions, for example. Up to 20% of people with diseases have genetic mutations that cause the misfolding. But about 80% of the cases are just sporadic misfolding of unknown cause. Also prion diseases are super rare--about 1 case in a million people. So prions in meat is a pretty low risk situation. What this study is showing is that classical prion proteins aren't the only ones that misfold and then get other proteins to misfold with them, causing disease in the process. Basically, what this group is saying is that "prion" is a much broader concept in biology--that many proteins beyond the mad cow ones can act like that.
Right now there are no drugs that stop or even slow Alzheimer's or Parkinson's. And that's not for a lack of trying. There have been several notable failures recently--drugs that went to clinical trials and showed no effects in patients. These drugs were designed before this idea that all these diseases were due to prionlike mechanisms started to pick up steam in the field. So now that there have been some fairly big papers suggesting that prionlike proteins are the cause, people can start looking at new designs for drugs that would stop prionlike propagation. Basically, people have already been doing that for classical prion diseases--making molecules that stop those proteins from aggregating into fibrils. So now drug makers could take all that's been learned with those molecules and apply them to Alzheimer's and Parkinson's.
Usually the compound in your pill is not the compound someone fished out of a microbe. It's been modified to give it better pharmacological properties--last longer in your bloodstream--and to avoid toxicity issues. So there is a lot of intellectual work that goes into making the compound you ingest even if the initial inspiration came from a fungus.
No one takes a molecule from a bacterium or fungus and then starts giving it to patients. You have to find the specific compound that allows the fungus/bacterium to kill its neighbors--a very labor intensive process. Then you have to get its structure. Then you test it to see if is druggable--will it last long enough in the bloodstream to be effective, for example. It probably isn't, so then you need to synthesize analogs and test them. Then you have to test it for toxicity, maybe synthesize more analogs to get around toxicity problems. And then you can start clinical trials--three rounds of them usually. Somewhere along the way you need to devise a way to make the compound in large enough quantities to turn it into a pill or injection or whatever deliverable form you're picking. So there are a lot of steps between "hey this compound from this fungus killed that bacteria," and "take this pill once a day for 10 days."
The use of the term reflects the usage by materials scientists. The titles of both papers describe the materials as 2-D. It is an established term in the field.
"a material in which the atomic organization and bond strength along two-dimensions are similar and much stronger than along a third dimension" REF: http://pubs.acs.org/doi/full/1....
Materials scientists use "two-dimensional" to describe graphene and similar materials. These are materials that consist of essentially a single molecular/atomic layer.
Really? How do they know it wasn't just raw sewage, or industrial chemicals if they didn't even identify the chemical, or even prove it came from the oil spill?
The PNAS paper that looked at the SF Bay spill ruled out sewage and other chemicals found in the Bay. They suggest sunlight transformed crude compounds into toxic ones. The PNAS paper is in front of a paywall, I believe: http://www.pnas.org/content/109/2/E51.full
Its not that the oil is "missed", its just that the oil once degraded to the point that it is not oil anymore is hard for them to measure with current methods, so they can't figure out where it went.
The main point, is that the oil is gone, degraded, oxidized, etc. The most dangerous (to marine life) part of the spill is gone.
But where degraded oil goes is a question scientists want to know, mainly because they don't fully understand what those compounds do to wild life. So even if the chemicals aren't the ones that originally spilled into the ocean, what they become is still of interest to researchers, because they know less about them.
They haven't identified specific compounds yet--sounds like that is next on their to-do list. The scientists definitely think the compounds arise after the oil spills out of the well and sits out in the sun for a bit. Basically you're right: They're talking about the end results of oil degradation. But the big question is what do these chemicals do to marine life. Are they toxic? Or do they just sit around and living things ignore them.
The particles get used up in the process, producing silicon oxides.
They make the nanoparticles from silane gas. The process is very energy intensive and produces CO2. So a pretty long tailpipe on this technology. You probably need more energy than you can create. Also it's unclear if these particles are better than magnesium hydride, which is the material of choice in many prototype fuel cells.