Comment Re:Huh? (Score 3, Insightful) 256
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.
Comment Re:3 people in 2 don't know math. (Score 1) 1042
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).
Comment Re:Great Until the Last 10 Minutes (Score 1) 955
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.
Submission + - BRCA1 and 2 gene patens are invalidated (nytimes.com)
Scubaraf writes: In a far-reaching ruling, Judge Robert W. Sweet anticipated a negative reaction from the industry. In a footnote of his 152-page ruling, he discounted fears that invalidating such patents would decimate the industry. ...the industry is already moving to a period of somewhat less dependence on DNA patents for its sustenance. Diagnostic laboratories, for instance, are shifting from testing individual genes to testing multiple genes or even a person’s entire genome. When hundreds or thousands of genes are being tested at once, patents on each individual gene can become a hindrance to innovation rather than a spur."
The basis of the decision is: "DNA being patented had long been considered a chemical that was isolated from, and different from, what was found in nature. But Judge Sweet ruled that the distinguishing feature of DNA is its information content, its conveyance of the genetic code. And in that regard, he wrote, the isolated DNA 'is not markedly different from native DNA as it exists in nature.'
The basis of the decision is: "DNA being patented had long been considered a chemical that was isolated from, and different from, what was found in nature. But Judge Sweet ruled that the distinguishing feature of DNA is its information content, its conveyance of the genetic code. And in that regard, he wrote, the isolated DNA 'is not markedly different from native DNA as it exists in nature.'
Submission + - McAfee: Google Attacks Not the Work of Amateurs (itworld.com)
itwbennett writes: McAfee says Damballa and other companies that followed up on McAfee's "Operation Aurura" research analyzed the wrong malware after McAfee provided wrong filenames. As a result, Damballa concluded that 'the Aurora attacks were the work of somewhat amateur botnet writers' and not the targeted and sophisticated attacks that McAfee was seeing, writes Robert McMillan. McAfee included four filenames in its original Aurora research that it now says are 'unrelated to Aurora and uses a different set of command and control servers,' McAfee Chief Technology Officer George Kurtz said in a Tuesday blog posting.
Submission + - Korea Becomes World's Biggest Malware Producer (net-security.org) 1
An anonymous reader writes: Korea now accounts for a massive 31.1 per cent of the world’s malware, a leap from February’s 8.9 per cent. This increase in Korean malware production is the result of the rise of compromised computers in Korea which are being used to send out phishing emails across the world. The US is the second most prolific producer of viruses, holding steady from February at 9.34 per cent. Next comes Brazil at 6.04 per cent, China at 5.05 per cent and India at 3.86 per cent.
Submission + - US wants commercial texting ban; public online say (networkworld.com) 1
coondoggie writes: The US Department of Transportation wants to not only ban texting by commercial bus and truck drivers, its also wants the public to get more closely involved developing transportation regulations via a new public Web site at Cornell University. On the texting issue, the department today announced a federal rule that aims to specifically prohibit texting by interstate commercial truck and bus drivers. The proposed rule would make permanent an interim ban announced in January 2010 that applied existing safety rules to the texting issue.
Comment Re:So (Score 3, Interesting) 260
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.
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.
Comment Re:scary (Score 1) 254
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.
Comment The message assumes prior knowledge of our world (Score 3, Interesting) 249
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.
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.
Comment Re:Intriguing. What about virus resistance? (Score 5, Insightful) 118
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.
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.
Comment How to solve the DNA migration rate problem! (Score 1) 90
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.
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.
Comment Re:Bound to fail (Score 1) 104
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.
Comment These are not the ants you are looking for... (Score 2, Interesting) 104
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.
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.
Comment Re:who would object? (Score 1) 198
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 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.
