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.

Admittedly off topic, but "happy with what they've got" is not a good metric for healthcare.If you are paying more for your care than you have to, getting more unnecessary or unproven (potentially harmful) procedures, getting less preventative care, and ending up with worse outcomes, then you are not getting a good deal. You may be happy with what you've got, but that does not mean that what you've got is good, especially when we have examples of countries spending less money for better outcomes while insuring everyone.

Notice I'm not arguing that we MUST do something about it, but stating that "being happy with it" is not a rational argument against trying to improve the system or even having to improve the system in order to ward off potentially disastrous consequences.

I call your metric the Bill Gates measure - paraphrased - "Everyone should be happy with 640K!"

I see one of the early tags is 'negligible.'

Maybe it is in terms of global CO2 levels, but under a cap and trade system, this will turn an industry that might have to buy CO2-emission rights into one that could make money selling them!

Congrats! That's a great story - as an oncologist, I hang on to each one these I hear (my colleague likes to say that melanoma gives cancer a bad name). The treatment you went through almost certainly stimulated your immune system to fight your cancer. It is not clear if this is a specific effect, where you actually teach the immune system to attack your tumor, or simply a stimulatory effect that revs up the immune system to do a better job of attacking tumor cells that it already had some reaction to.

As you know, our only approved immune therapy for melanoma is interferon - a non-specific stimulator of immunity. There are few responders, but a small fraction (1-4%), are actually cured or disease free for years. The rest have little or no response and the side effects can be brutal or even fatal. The same goes for high dose interleukin-2 therapy for metastatic renal cell carcinoma - this treatment is usually started in an ICU setting.

The more specific cancer vaccines are always given with powerful adjuvants or co-stimulatory products. Provenge is a great example of this - some responders, but not clear what they are responding to. My Dad was in a clinical trial with a different prostate cancer vaccine and is a responder! In his case, he got the vaccine in highly immunogenic vectors - vaccinia (weak small pox, essentially) and fowlpox. This was followed by co-injection of GM-CSF - a chemotactic growth factor for a variety of antigen presenting cells. He isn't cured, but has stable disease. It's not clear if his immune system responded to the specific antigen in the vaccine or simply amplified whatever endogenous anti-tumor activity it already had brewing.

So - without bashing the achievement cited in the article - I suspect that this will not have anywhere near the impact the article claims. We certainly aren't going to be abandoning screening colonoscopy as the article suggests.

While I laud this development - we have had multiple form of immune therapy for cancer - including tumor vaccines, cancer antigen vaccines, immunostimulatory drugs, and anti-tolerance drugs for years now. There are some responders, but this field has generally been a disappointment. here's to hoping we eventually figure out how to harness this approach.

I came to agree with the toolittletoolate tag. I was seriously gearing up to buy a Kindle, but the broken-by-design and big-brother "features" that have now moved from theoretical to actual have convinced me to stay far away from this product.

I'll wait until the DRM issues have shaken out (as they have largely done with music) before considering a company-yoked product like this.

The pinhole camera on an iPhone has an aperture smaller than the human pupil.

This works easily, on regular microscopes, without any special attachment.
A regular microscope is going to be much more versatile.

I'll have to read the PLoS Online article to see what I'm missing.

And you would have to lift the plates back up or use a conveyor belt which would erode the energy gains.