Your implication is the his lack of experience led to the adoption of policies that you don't agree with. That's hardly a condemnation of his ability to be president. Overall, his approval ratings are far better the GWB's at the end of his second term - a guy who at that point had plenty of executive experience.
Obama also had no military experience and little foreign policy experience, yet even most conservatives think that he is doing well on the "war on terror."
I agree with your last point, but experience is overrated in a presidential candidate. They bring a team with them and their ability to succeed in a primary and federal election is a reasonable proof of basic competence. Now, if a candidate has experience running a large organization and seriously screwed it up, that's another issue.
Unless you never circulate the coin and melt it down once the debt level falls below that of the debt ceiling.
The point is that the debt ceiling is a made up limit. Most countries don't have one.
Increasing this arbitrary limit does not let us spend more money - it allows us to BORROW more money in order to pay for those things that we already bought!
In other words, the fight we're having over the debt ceiling now should have taken place over the BUDGET. That's were the spending decisions take place. By not raising the debt ceiling now, all we are saying is that we won't pay back the money we HAVE ALREADY SPENT. That sends a bad message to those that might lend us money in the future - raising our rates - and actually makes us SPEND MORE MONEY in the future to service our debt.
If you want to reduce the deficit, fix the budget (more revenues, less spending). Don't shoot yourself in the foot as a punishment for already having spent more money that you have in the hopes that it will force you to budget better next time.
Sure you have to do a complicated dance routine to flip through channels and change the volume, but maybe, one day soon, we'll be able to operate basic television controls from across the room using only a single thumb!
Wake when my TV can figure out what I want to watch and puts it on before my ass hits the couch.
It doesn't quite work that way, but the answer to your question is that the database is stored in the DNA of immune cells.
Essentially, the newborn cells of the adaptive immune system (B and T-cells) undergo rearrangements of their DNA to produce a incredibly wide variety of receptors.
Then, they go through a selection process - if they react strongly with self, they die (negative selection). After a few more maturation and selection steps, the surviving immune cells are sent throughout the body.
If one of them later binds strongly to something (which is presumably foreign) in the right context, they activate. They trigger an immune response and proliferate. A subset of these daughter cells become essentially immortal - outlasting the immune response they fought in, but ready to quickly mobilize should that foreign substance be encountered again.
So, the memory cells are the hardware, but the rearranged antigen receptor gene they harbor is the information they need to work.
But that's a huge point to prove. As obvious as it may sound, it's evidence that validating patients and their concerns may be among the best things we can do as physicians. It's absolutely not billable, so many docs don't do it - instead focusing on seeing the next person quickly or doing another billable procedure.
Maybe with more studies aimed at understanding the effect of doctor-patient interactions, we'll start reimbursing MD's for what works and patients find valuable.
But he has a point. Several psychiatric drugs have been shown to be no better or worse than placebo. We didn't hear about it because these negative trials were suppressed by the drug companies. They only published the positive ones - do enough studies and one will work!
Even the open placebo used in this study appeared as good as the leading therapy for IBS (although they weren't compared head-to-head).
This is fascinating to me.It proves how much we don't know about how people work.
As a physician I have on several occasions wanted to prescribe a placebo, knowing that time would be the best remedy and that simply feeling like the patient is doing something might improve their outlook immediately. Of course, I consider that misleading and unethical. To know that it might work even if you are up front about it is amazing. I'm not sure that it would work outside of a clinical trial though. I'd love to know how/if it really works.
Several possibilities -
1) Just a statistical fluke - it won't be born out in repeat studies.
2) Specific only to disorders like IBS which has a highly variable course, subjective symptoms, and is hard to diagnose. This isn't going to work with leukemia.
3) An example of "active" intervention where a person feels like they are being helped to help themselves even if they cognitively don't believe it. It's what underlies the "healing touch" in medicine and maybe even the power of meditation/prayer (praying for yourself that is, not being in a coma and having others pray for you).
I also don't know how they got the study past the scientific review board, which I thought, would laugh them out of the room.
Then education would work like the media does today. The loudest or hottest or most in-line with what you already think "professors" would dominate those that actually know more about their field. You wouldn't be learning as much as concreting your world view - exactly the opposite of what higher education should do.
In fact, why not skip the university concept and meld education into the media entirely? Sign me up for the Daily Show Community College.
Retarded headline. It would be as valid to analyze his iPhone to see how electronics deal with toxins.
Sequencing his genome is a publicity stunt. Nothing more.
There are 10 types of people in the world, those who understand n base numbering system, those who don't, those who think it is n-1 base system, those who think it is n-2 base system,... , and those who mistake it for binary (n-k=2).
Re:Great Until the Last 10 Minutes
on
Lost Ends
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· Score: 1
This is exactly where I hoped they were going. Ben Linus was a perfect example of that. He was an shit person - a total manipulative, scheming opportunist with no morality. Yet even he redeems himself to some degree. The writers could have made it more obvious - saying that Linus is staying to atone for kidnapping the Frenchwoman's daughter and letting her die later on - that he needed to reconcile with his father - and the like.
It would have been nice to know that these richly developed characters still had life to live with the benefit of who they had become after their time on the Island.
The cancer concern is a legitimate one. These p21 knockouts are lab mice kept in clean conditions. They may not develop cancers in a three year span, but that demonstrates little about the oncogenic potential in humans.
I'm assuming there is some evolutionary reason for curtailing a vigorous healing response. It maybe to reduce the cancer rate, but it could just as simply be something else very important - regulation of immune response for example.
One potentially useful experiment would be to challenge these mice with carcinogen (like ENU) and see what their cancer rate is compared to controls. Alternatively, you could use genetic means (insertion of oncogenes or mating to mice with knocked out tumor suppressor genes) to see if the cancers they develop are more aggressive or more likely to metastasize.
In any case, this is a very cool finding.
Exactly! I'm not sure how you go from RF to decreased beta-amyloid deposition, but a plausible mechanism for dysregulating gene expression has been proposed. Namely, RF can disrupt the hydrogen bonds that anneal complimentary strands of DNA together. This can have many effects including unsilencing genes, interference with DNA replication (and thereby increasing the mutation rate), and interference with mRNA synthesis - all without ionizing a damn thing.
Sending out a DNA sequence assumes that the receiver understands a great deal about our planet and the molecular basis of life on it.
Think about it, even if they understood the message was about DNA, they would have to know our amino acid code in order to interpret it as the template for a protein. A protein that either did not evolve on their world, or evolved in a completely different way.
In effect, all we saying with this message is that we have advanced enough to recognize that DNA is the basis for life on this planet. Only a sentience that already understood that basis could interpret this message.
It's akin to someone shouting, "a-squared + b-squared = c-squared!" - out-of-context - in the antarctic. It shows you have learned something, but there either isn't anyone to hear you or they won't understand you unless they knew all about you (and Euclidian geometry) already.
Now you know how I feel when there's an article about API's, Ubuntu, or codecs.
Human cells have and express p16-INK4A normally - it's part of the CDKN2A gene locus. It is a cell cycle control gene whose main function is to put the brakes on replication. p16 is expressed in human cells and is often mutated or outright deleted in many human cancers of all cell types. COSMIC (new window)
The difference described in naked mole rats is that their cells induce p16 expression after minimal contact with neighboring cells while human and rat cells need more prodding to turn on cell cycle control genes.
This is a cool finding, but does not have a direct application in human cancers anytime soon. It's very hard to turn on a gene that has been mutated or deleted in cancer cells. You have to do it in practically every cell, otherwise, they grow back. Even then it may be too late. Loss of contact inhibition may be necessary in early oncogenesis, but restoration of p16 expression in a cancer cell that already has multiple genetic mutations, may not do much at that point. So, it's an interesting finding and I hope it leads to a better understanding of cancer and cancer prevention. But honestly, we have cool findings like this once a week. It just requires the right spin to sell it to the media - like calling something a "cancer-proof" gene - and it finds its way here.
It sounds like the major problem with this technology is controlling the rate of passage of a single DNA strand through the detection pore. Instead of trying to solve that "hard" problem, why not design the system so that you don't need such tight control over the speed of the DNA strand?
In the current system, if the strand moves to slowly between reads, a base will be scanned twice. If the strand moves too quickly, some bases may be skipped altogether. You could slow down the rate of strand passage relative to the scanning frequency, but then you couldn't differentiate between a sequence of 3 G's in a row or a single G getting scanned three times.
If you design your DNA reader with multiple reading points in series (i.e. read the strand simultaneously at multiple points along it's length), this problem would go away. Here's how it works:
1. You assume that the entire strand moves at the same rate (this rate can vary, but must be slow compared to the scan rate of the base readers).
2. If any of your serial DNA readers record a change in base, you interpret this to mean that the DNA molecule has moved down the pore by one base height. Any detectors that did not record a base change are likely reading their next base as well, but it just happens to be the same kind as the one they read just prior.
By allowing for multiple scans per base, you increase the likelihood of making a correct call. In fact, you may be able to distinguish a C from a methyl-C from a hydroxymethyl-C and get epigenetic information at the same time you get sequence information! By using multiple detectors in series, you are able to detect when the DNA strand has moved one base height and get another crack at making sure you read the right bases.
If anyone from IBM sees this and thinks it might work - drop me a note. I would be very interested in participating in the development/testing of this technology.
- Cancer genetics researcher / clinician.
The scent signal only travels so far. This will not create a defense void at the side opposite the infection. But, the "ants" should not only lay down scent trails when they pick up a threat, they should clone themselves. This will select for the repertoire of ants than can identify this type of threat. That way you bring more effort to bear at the site of infections with out worrying about depleting resources on the "other side" of the network. Once the initial threat is over, the cloned ants disperse, covering the whole network. The system is now effectively inoculated against this specific type of threat - with the latency to respond to a subsequent attack significantly decreased. All without user intervention.
Ants are not a good analogy. What they are describing is much more like an adaptive immune system - the "ants" in their system are circulating T-cells. Dr. Rodney Langman, an immunologist from the Salk Institute and UCSD, proposed exactly what the article describes. He described the conceptual elements required to form a synthetic immune system in the early 90's. Initially the goal was to model and understand our own adaptive immunity, but he often used computers and network protection from viruses as examples when explaining the concepts. I was his TA while in grad school.
If we extrapolate - computer networks will not only be guarded by T-cells that circulate through networks, identify threats, and release proinflammatory markers and antiviral "poisons" - there will be B-cell equivalents that produce antibodies, snippets of code the bind and immobilize specific codes they are designed to recognize. There will also be some degree of autoimmunity as viruses are reworked to mimic benign code. There will be an HIV equivalent (there already are) that targets not just the OS, but the OS defenses themselves. And there will be vaccines - benign code that presented as a virus to train the immune system on a specific type of threat.
It's not an inoculation for being wrong on this subject, but I'm a cancer researcher with a BS in physics, so I have some "exposure" to this topic.
The alpha particles do pass cell membranes (mammalian cells don't have walls) - cell membranes are only 3-5 nm thick and the mean free path of uranium-decay alpha particles (4.3MeV) is much greater than that, even in water. But they don't have to to get into cells to cause damage since uranium and other radioactive elements can be internalized into cells and can form precipitates and can concentrate in bones. Nor does an alpha particle have to hit DNA to cause genetic damage. The particle carries a naked +2 charge and will quickly cause ionization events which that propagate by creating secondary ionization events. The net result is free-radical formation and disruption of molecular bonds. This leads to cell death or mutation and subsequent risk of cancer.
There are multiple examples of alpha-particle induced biologic damage, such as chronic exposure to Radon (an alpha-emitter) which has been linked to cancer. That said, Uranium itself has a very long half-life and is more likely to be damaging by being toxic than by being radioactive at levels found in the environment.
The risk of uranium in the air is not that it will release alpha particles that will travel miles and kill people. The problem is that the uranium will be inhaled or ingested, become incorporated into people's bodies, and then release alpha particles that are very likely to interact (as your post correctly indicates they will) with the molecular constituents of cells. Exposure to external alpha-emitters is safe, but internalization can cause cancer (or be acutely devastating, depending on the dose - see Litvinenko and Po-210, an alpha-emitter). That and the fact that thorium and uranium are toxic heavy metals independent of their radioactivity.
I don't know what the average monthly bill is for electricity in Japan, but assuming a measly $200 per month, this thing would have to last 29 years just to break even! And that ignored maintenance costs and likely overruns!
If it works, it's a great proof of concept - and something you can sell to other nations once the costs come down.
Slashdot Mirror
"SoundWave has detected that you are trying to masturbate. Shall I redirect your browser to a porn site appropriate for your sexual orientation?"
Clippy
Your implication is the his lack of experience led to the adoption of policies that you don't agree with. That's hardly a condemnation of his ability to be president. Overall, his approval ratings are far better the GWB's at the end of his second term - a guy who at that point had plenty of executive experience.
Obama also had no military experience and little foreign policy experience, yet even most conservatives think that he is doing well on the "war on terror."
I agree with your last point, but experience is overrated in a presidential candidate. They bring a team with them and their ability to succeed in a primary and federal election is a reasonable proof of basic competence. Now, if a candidate has experience running a large organization and seriously screwed it up, that's another issue.
Unless you never circulate the coin and melt it down once the debt level falls below that of the debt ceiling.
The point is that the debt ceiling is a made up limit. Most countries don't have one.
Increasing this arbitrary limit does not let us spend more money - it allows us to BORROW more money in order to pay for those things that we already bought!
In other words, the fight we're having over the debt ceiling now should have taken place over the BUDGET. That's were the spending decisions take place. By not raising the debt ceiling now, all we are saying is that we won't pay back the money we HAVE ALREADY SPENT. That sends a bad message to those that might lend us money in the future - raising our rates - and actually makes us SPEND MORE MONEY in the future to service our debt.
If you want to reduce the deficit, fix the budget (more revenues, less spending). Don't shoot yourself in the foot as a punishment for already having spent more money that you have in the hopes that it will force you to budget better next time.
There is an open source DNA sequencing project out there: http://www.polonator.org/
But the fact is that it is still expensive as a hobby.
Love it! I'm in for one.
Combine it with the kinect so all you have to do is sit down and I'll buy two.
Sure you have to do a complicated dance routine to flip through channels and change the volume, but maybe, one day soon, we'll be able to operate basic television controls from across the room using only a single thumb!
Wake when my TV can figure out what I want to watch and puts it on before my ass hits the couch.
It doesn't quite work that way, but the answer to your question is that the database is stored in the DNA of immune cells.
Essentially, the newborn cells of the adaptive immune system (B and T-cells) undergo rearrangements of their DNA to produce a incredibly wide variety of receptors.
Then, they go through a selection process - if they react strongly with self, they die (negative selection). After a few more maturation and selection steps, the surviving immune cells are sent throughout the body.
If one of them later binds strongly to something (which is presumably foreign) in the right context, they activate. They trigger an immune response and proliferate. A subset of these daughter cells become essentially immortal - outlasting the immune response they fought in, but ready to quickly mobilize should that foreign substance be encountered again.
So, the memory cells are the hardware, but the rearranged antigen receptor gene they harbor is the information they need to work.
Bingo!
But that's a huge point to prove. As obvious as it may sound, it's evidence that validating patients and their concerns may be among the best things we can do as physicians. It's absolutely not billable, so many docs don't do it - instead focusing on seeing the next person quickly or doing another billable procedure.
Maybe with more studies aimed at understanding the effect of doctor-patient interactions, we'll start reimbursing MD's for what works and patients find valuable.
But he has a point. Several psychiatric drugs have been shown to be no better or worse than placebo. We didn't hear about it because these negative trials were suppressed by the drug companies. They only published the positive ones - do enough studies and one will work!
Even the open placebo used in this study appeared as good as the leading therapy for IBS (although they weren't compared head-to-head).
This is fascinating to me.It proves how much we don't know about how people work.
As a physician I have on several occasions wanted to prescribe a placebo, knowing that time would be the best remedy and that simply feeling like the patient is doing something might improve their outlook immediately. Of course, I consider that misleading and unethical. To know that it might work even if you are up front about it is amazing. I'm not sure that it would work outside of a clinical trial though. I'd love to know how/if it really works.
Several possibilities -
1) Just a statistical fluke - it won't be born out in repeat studies.
2) Specific only to disorders like IBS which has a highly variable course, subjective symptoms, and is hard to diagnose. This isn't going to work with leukemia.
3) An example of "active" intervention where a person feels like they are being helped to help themselves even if they cognitively don't believe it. It's what underlies the "healing touch" in medicine and maybe even the power of meditation/prayer (praying for yourself that is, not being in a coma and having others pray for you).
I also don't know how they got the study past the scientific review board, which I thought, would laugh them out of the room.
What if we ran universities like Wikipedia?
Then education would work like the media does today. The loudest or hottest or most in-line with what you already think "professors" would dominate those that actually know more about their field. You wouldn't be learning as much as concreting your world view - exactly the opposite of what higher education should do.
In fact, why not skip the university concept and meld education into the media entirely? Sign me up for the Daily Show Community College.
Daddy - why didn't our ancestors start working on a way to colonize the solar system before the Sun started expanding?
Because your great-great-great-great-google-grandpa was really into NASCAR and porn and couldn't spare the dough to fund our species-saving research.
Oh - I see. I'm glad he had his priorities straight. The entire sum of human existence shouldn't be forgotten for nothing, you know?
Retarded headline. It would be as valid to analyze his iPhone to see how electronics deal with toxins. Sequencing his genome is a publicity stunt. Nothing more.
There are 10 types of people in the world, those who understand n base numbering system, those who don't, those who think it is n-1 base system, those who think it is n-2 base system, ... , and those who mistake it for binary (n-k=2).
This is exactly where I hoped they were going. Ben Linus was a perfect example of that. He was an shit person - a total manipulative, scheming opportunist with no morality. Yet even he redeems himself to some degree. The writers could have made it more obvious - saying that Linus is staying to atone for kidnapping the Frenchwoman's daughter and letting her die later on - that he needed to reconcile with his father - and the like. It would have been nice to know that these richly developed characters still had life to live with the benefit of who they had become after their time on the Island.
The cancer concern is a legitimate one. These p21 knockouts are lab mice kept in clean conditions. They may not develop cancers in a three year span, but that demonstrates little about the oncogenic potential in humans.
I'm assuming there is some evolutionary reason for curtailing a vigorous healing response. It maybe to reduce the cancer rate, but it could just as simply be something else very important - regulation of immune response for example.
One potentially useful experiment would be to challenge these mice with carcinogen (like ENU) and see what their cancer rate is compared to controls. Alternatively, you could use genetic means (insertion of oncogenes or mating to mice with knocked out tumor suppressor genes) to see if the cancers they develop are more aggressive or more likely to metastasize. In any case, this is a very cool finding.
Exactly! I'm not sure how you go from RF to decreased beta-amyloid deposition, but a plausible mechanism for dysregulating gene expression has been proposed. Namely, RF can disrupt the hydrogen bonds that anneal complimentary strands of DNA together. This can have many effects including unsilencing genes, interference with DNA replication (and thereby increasing the mutation rate), and interference with mRNA synthesis - all without ionizing a damn thing.
Sending out a DNA sequence assumes that the receiver understands a great deal about our planet and the molecular basis of life on it.
Think about it, even if they understood the message was about DNA, they would have to know our amino acid code in order to interpret it as the template for a protein. A protein that either did not evolve on their world, or evolved in a completely different way.
In effect, all we saying with this message is that we have advanced enough to recognize that DNA is the basis for life on this planet. Only a sentience that already understood that basis could interpret this message.
It's akin to someone shouting, "a-squared + b-squared = c-squared!" - out-of-context - in the antarctic. It shows you have learned something, but there either isn't anyone to hear you or they won't understand you unless they knew all about you (and Euclidian geometry) already.
Now you know how I feel when there's an article about API's, Ubuntu, or codecs.
Human cells have and express p16-INK4A normally - it's part of the CDKN2A gene locus. It is a cell cycle control gene whose main function is to put the brakes on replication. p16 is expressed in human cells and is often mutated or outright deleted in many human cancers of all cell types.
COSMIC (new window)
The difference described in naked mole rats is that their cells induce p16 expression after minimal contact with neighboring cells while human and rat cells need more prodding to turn on cell cycle control genes.
This is a cool finding, but does not have a direct application in human cancers anytime soon. It's very hard to turn on a gene that has been mutated or deleted in cancer cells. You have to do it in practically every cell, otherwise, they grow back. Even then it may be too late. Loss of contact inhibition may be necessary in early oncogenesis, but restoration of p16 expression in a cancer cell that already has multiple genetic mutations, may not do much at that point. So, it's an interesting finding and I hope it leads to a better understanding of cancer and cancer prevention. But honestly, we have cool findings like this once a week. It just requires the right spin to sell it to the media - like calling something a "cancer-proof" gene - and it finds its way here.
It sounds like the major problem with this technology is controlling the rate of passage of a single DNA strand through the detection pore. Instead of trying to solve that "hard" problem, why not design the system so that you don't need such tight control over the speed of the DNA strand?
In the current system, if the strand moves to slowly between reads, a base will be scanned twice. If the strand moves too quickly, some bases may be skipped altogether. You could slow down the rate of strand passage relative to the scanning frequency, but then you couldn't differentiate between a sequence of 3 G's in a row or a single G getting scanned three times.
If you design your DNA reader with multiple reading points in series (i.e. read the strand simultaneously at multiple points along it's length), this problem would go away. Here's how it works:
1. You assume that the entire strand moves at the same rate (this rate can vary, but must be slow compared to the scan rate of the base readers).
2. If any of your serial DNA readers record a change in base, you interpret this to mean that the DNA molecule has moved down the pore by one base height. Any detectors that did not record a base change are likely reading their next base as well, but it just happens to be the same kind as the one they read just prior.
By allowing for multiple scans per base, you increase the likelihood of making a correct call. In fact, you may be able to distinguish a C from a methyl-C from a hydroxymethyl-C and get epigenetic information at the same time you get sequence information! By using multiple detectors in series, you are able to detect when the DNA strand has moved one base height and get another crack at making sure you read the right bases.
If anyone from IBM sees this and thinks it might work - drop me a note. I would be very interested in participating in the development/testing of this technology. - Cancer genetics researcher / clinician.
The scent signal only travels so far. This will not create a defense void at the side opposite the infection. But, the "ants" should not only lay down scent trails when they pick up a threat, they should clone themselves. This will select for the repertoire of ants than can identify this type of threat. That way you bring more effort to bear at the site of infections with out worrying about depleting resources on the "other side" of the network. Once the initial threat is over, the cloned ants disperse, covering the whole network. The system is now effectively inoculated against this specific type of threat - with the latency to respond to a subsequent attack significantly decreased. All without user intervention.
Ants are not a good analogy. What they are describing is much more like an adaptive immune system - the "ants" in their system are circulating T-cells. Dr. Rodney Langman, an immunologist from the Salk Institute and UCSD, proposed exactly what the article describes. He described the conceptual elements required to form a synthetic immune system in the early 90's. Initially the goal was to model and understand our own adaptive immunity, but he often used computers and network protection from viruses as examples when explaining the concepts. I was his TA while in grad school.
Synthetic Immunity
If we extrapolate - computer networks will not only be guarded by T-cells that circulate through networks, identify threats, and release proinflammatory markers and antiviral "poisons" - there will be B-cell equivalents that produce antibodies, snippets of code the bind and immobilize specific codes they are designed to recognize. There will also be some degree of autoimmunity as viruses are reworked to mimic benign code. There will be an HIV equivalent (there already are) that targets not just the OS, but the OS defenses themselves. And there will be vaccines - benign code that presented as a virus to train the immune system on a specific type of threat.
It's not an inoculation for being wrong on this subject, but I'm a cancer researcher with a BS in physics, so I have some "exposure" to this topic.
The alpha particles do pass cell membranes (mammalian cells don't have walls) - cell membranes are only 3-5 nm thick and the mean free path of uranium-decay alpha particles (4.3MeV) is much greater than that, even in water. But they don't have to to get into cells to cause damage since uranium and other radioactive elements can be internalized into cells and can form precipitates and can concentrate in bones. Nor does an alpha particle have to hit DNA to cause genetic damage. The particle carries a naked +2 charge and will quickly cause ionization events which that propagate by creating secondary ionization events. The net result is free-radical formation and disruption of molecular bonds. This leads to cell death or mutation and subsequent risk of cancer.
There are multiple examples of alpha-particle induced biologic damage, such as chronic exposure to Radon (an alpha-emitter) which has been linked to cancer.
That said, Uranium itself has a very long half-life and is more likely to be damaging by being toxic than by being radioactive at levels found in the environment.
The risk of uranium in the air is not that it will release alpha particles that will travel miles and kill people. The problem is that the uranium will be inhaled or ingested, become incorporated into people's bodies, and then release alpha particles that are very likely to interact (as your post correctly indicates they will) with the molecular constituents of cells. Exposure to external alpha-emitters is safe, but internalization can cause cancer (or be acutely devastating, depending on the dose - see Litvinenko and Po-210, an alpha-emitter). That and the fact that thorium and uranium are toxic heavy metals independent of their radioactivity.
Agreed! It comes out to 71K per household!
I don't know what the average monthly bill is for electricity in Japan, but assuming a measly $200 per month, this thing would have to last 29 years just to break even! And that ignored maintenance costs and likely overruns!
If it works, it's a great proof of concept - and something you can sell to other nations once the costs come down.