Slashdot Mirror

Here's a radical idea I heard about: let's domesticate everything remotely domesticable. After all, cats and dogs aren't going to go extinct any time soon. I'm pretty sure that quite a few species like red pandas could make very viable pets. In fact they're probably endangered by their protection status. Who wouldn't want to have something this cute? Allow people to keep them, and they'll get bred like rabbits. Videos like this one suggest that they'd make pretty fun pets.

For breeds that are too large, breed them down to a manageable size (if we can make a chihuahua surely we can make a dog sized tiger).

Experiments with foxes seem to show that domestication is quite possible in a reasonable amount of time, and research shows that only 40 genes seem to be responsible for the domestication.

So, here's the idea: domesticate everything, study what changed in the genetics, and if the wild population decays too much, use the genetics research to reverse the domestication, while drawing from the abundant pet population.

I think that this might be the better solution long term, as maintaining habitats and populations is a never ending struggle, while that is never a problem for any species people have an use for.

You'll probably be interested in this paper.

Discussion of producing neural progenitors from both hESC and hiPSC. Touches on the different types which can be produced, production methods, and issues faced in production.

And what about that one http://www.cell.com/abstract/S0092-8674(11)00132-2? This debate is far from being settled.

It's simply survival of the fittest. At the turn of the century, nanotubes and buckyballs were "cool" academically. Now it's graphene. Though these have been around since 60 years (see the 1947 paper The Band Theory of Graphite ).

I agree that fads are fads, but this is how science will progress from hereon. It used to be a practice of a handful of people in the early days, even towards the first half of the 20th century. Academic research now is a valid career option for a large number of people. Just like any other career, it has certain "return on investments". The ROI's in this case are papers, patents and awards. This IS the yardstick with which your success is measured in the scientific field. It goes to logic people are going to try and stay at the top of their game by going after "modern" and "cutting-edge" topics.

I wouldn't completely agree with your argument of only a few applications remaining. I am not an expert on buckyballs, so I'll refrain from commenting on that, but for Carbon Nanotubes (CNT) there are an insane number of applications already in place. They range from CNT based logic, radio, Atomic force microscopy etc (too many to fit here)

Scientific (or otherwise in the BBC case) media will always glamorize any scientific discovery and exaggerate its potential, as it does for everything else. This is not necessarily an issue with the scientific community who does the research work. If anything, media stories like these end up slapping unreal expectations on scientists and engineers. This ultimately results in a "disappointment" on the public's side when all the proclaimed applications are not realized and electronics industry still runs on Silicon.

Paywall to download, but here is the original publication. At my work, we have a site subscription to many journals including this one. There may be a free source out there but I couldn't find it. http://download.cell.com/neuron/pdf/PIIS0896627311001607.pdf

The DCA Site website was put up by laymen to pool together scarce information due to the lack of knowledge available at the time what research was available from corporate or academic sources.

You'll find similar inaccuracies in exact terminology or phrasing in the laymen comments on The DCA Site as you can find in laymen comments in Slashdot. I doubt that the intent was to convey that the mitochondria was completely disabled, only that an important function of the mitochondria, the ability to signal time for cell death, was disabled in cancer cells. Also, the poster was not conveying an opinion, he is citing a paper so that you can look into it further.

http://www.cell.com/cancer-cell/abstract/S1535-6108(06)00372-2

Here's an excerpt from WIki:

"Cancer cells generally use glycolysis rather than respiration (oxidative phosphorylation) for energy (the Warburg effect), as a result of hypoxia that exists in tumors and damaged mitochondria.[13] Usually dangerously damaged cells kill themselves via apoptosis, a mechanism of self-destruction that involves mitochondria, but this mechanism fails in cancer cells.

A phase one study published in January 2007 by researchers at the University of Alberta, who had tested DCA on cancer cells grown in mice, found that DCA restored mitochondrial function, thus restoring apoptosis, killing cancer cells and shrinking the tumors.[14]"

http://en.wikipedia.org/wiki/Dichloroacetic_acid

= 9J =

There are pictures in the journal article they cite: http://download.cell.com/neuron/pdf/PIIS089662731000766X.pdf?intermediate=true

http://www.cell.com/current-biology/fulltext/S0960-9822(10)01020-1?large_figure=true

Or maybe induced pluripotent stem (iPS) cells which are reprogrammed, acquire more telomere transcripts which elongate the telomeres... Or maybe not... Who really knows for sure...

http://www.cell.com/cell-stem-cell/abstract/S1934-5909(09)00002-2

Summary
Telomere shortening is associated with organismal aging. iPS cells have been recently derived from old patients; however, it is not known whether telomere chromatin acquires the same characteristics as in ES cells. We show here that telomeres are elongated in iPS cells compared to the parental differentiated cells both when using four (Oct3/4, Sox2, Klf4, cMyc) or three (Oct3/4, Sox2, Klf4) reprogramming factors and both from young and aged individuals. We demonstrate genetically that, during reprogramming, telomere elongation is usually mediated by telomerase and that iPS telomeres acquire the epigenetic marks of ES cells, including a low density of trimethylated histones H3K9 and H4K20 and increased abundance of telomere transcripts. Finally, reprogramming efficiency of cells derived from increasing generations of telomerase-deficient mice shows a dramatic decrease in iPS cell efficiency, a defect that is restored by telomerase reintroduction. Together, these results highlight the importance of telomere biology for iPS cell generation and functionality.

Seems OK here:

http://www.cell.com/abstract/S0092-8674(10)00938-4

so... I read the summary and they don't seem to say why this extra zinc is there in disease patients.

http://www.cell.com/retrieve/pii/S0092867404002089 Wagers, A.G., and Weissman, I.L. 2004. Plasticity of Adult Stem Cells. Cell 116(5):639-648.

Now, iPS cells are a promise, but they are a lot more difficult to induce and work with compared to natural pluripotent cells (aka embryonic).
Nishikawa, S., Goldstein, R.A., Nierras, C.R. 2008. The promise of human induced pluripotent stem cells for research and therapy. Nature Reviews Molecular Cell Biology. 9:725-729.

Image Reconstruction from Brain Activity.

video, article

In an experiment, a group of children with Williams syndrome showed no signs of inherent racial bias, unlike children without the syndrome.

http://www.cell.com/current-biology/fulltext/S0960-9822(10)00144-2

Interesting link, thanks. I do think however it reinforces what I was saying about it being more societal than genetic. While the kids with Williams definitely showed no bias and those without did, the study points out that this appears to be that Williams blocks these biases from forming (societally) rather than the biases themselves being genetic in nature.

I don't think that in this context "racism" necessarily means what it might generally mean. I believe they often measure it in babies by seeing how long a baby will remain interested on average by pictures of various faces of people with various ethnicities. It's not about the babies thinking "any less" of anyone, it's just some sort of hard-coded response. Anyways, I'm not a biologist or anything, so I'm not really qualified to disect that paper, though I've seen various similar ones in some other journals.

The baby thing would be nice to have a link for if you've got one. I'd like to know if these babies have any kind of social imprinting or not prior to the tests. In my understanding babies do imprint VERY quickly to their parents for example. And, for extra confirmation, if caucasian babies born in a non-caucasian society that never got to see their own parents (and thus surrounded by non-caucasian doctors and nurses) will have biases that are based on their own race, their surroundings, or neither. Sadly, while such babies would be invaluable for this research, it's pretty rare to find those exact circumstances and probably a fairly large ethical problem to deliberately create such circumstances in sufficiently large sample sizes to be useful...

In an experiment, a group of children with Williams syndrome showed no signs of inherent racial bias, unlike children without the syndrome.

http://www.cell.com/current-biology/fulltext/S0960-9822(10)00144-2

I don't think that in this context "racism" necessarily means what it might generally mean. I believe they often measure it in babies by seeing how long a baby will remain interested on average by pictures of various faces of people with various ethnicities. It's not about the babies thinking "any less" of anyone, it's just some sort of hard-coded response. Anyways, I'm not a biologist or anything, so I'm not really qualified to disect that paper, though I've seen various similar ones in some other journals.

"SOME biologists and neuroscientists will always be around who say what you want. If you can show that the mainstream opinion is against me, I'll happily concede the point, and thank you for enlightening me, but I doubt it."

Some studies of insect locomotion (which was where this discussion started) which use experimental data, modelling, or a mixture of the two to show that a great deal of locomotion sensing and control happens either in the limbs themselves before they reach any nerve centres, or in the thoracic ganglia. Nerve stimulation experiments have also shown that the characteristic "dual tripod" gait of hexapods is a mechanical oscillatory cycle that runs automatically when single nerves in the brain or mesothoracic ganglia are stimulated. The same is true for wing beats (which is some types share both muscles and central ganglia with the legs), which will cycle repeatedly when nerves in the thoracic ganglia are stimulated. The notable similarity in the data gathered from not only animals of the same species, but but those of different but closely related ones indicates that these movements are produced by a fixed "hardware" pattern generator, similar in principle to the electro-mechanical sequencers used in dishwashers and washing machines before microprocessor control became common:

(Note I apologise in advance for some of these only abstracts. Full scientific papers and book texts are hard to find on the web):

http://jn.physiology.org/cgi/content/full/82/1/512
http://www3.interscience.wiley.com/journal/45436/abstract

http://pt.wkhealth.com/pt/re/ejnr/abstract.00009274-200419070-00019.htm;jsessionid=KwpKVK0J1jTLRRXsZmb2QJJ53LlxD8s1Tnhv6l5Fqj9qNF2ncS7l!-1104825961!181195629!8091!-1

http://www.nature.com/nature/journal/v283/n5749/abs/283768a0.html

http://www3.interscience.wiley.com/journal/109692463/abstract

http://www.cell.com/biophysj/abstract/S0006-3495(65)86706-6

http://209.85.229.132/search?q=cache:5jTmyj1E8ywJ:biology.queensu.ca/~locust/Publications/locust%2520flight.pdf+insect+proprioceptors+ganglia&cd=75&hl=en&ct=clnk

"Oh really? You read it's mind then?"

There is absolutely no evidence that insects have anything that fits the description of a "mind" to read. Note though that some spiders may well have minds, e.g. Portia labiata, which displays a level of intelligence that makes many small mammals look like warm-blooded morons.

"Humans are predictable too. Doesn't mean they're not intelligent. They're just creatures of habit."

Humans are predictable en-masse, but not individually. Most insects on the other hand are entirely predictable individually, i.e. they always react in precisely the same way to the same sets of stimuli as another insect of the same species.

"Well, Jellyfish ARE pretty dumb, you know. The most complex behaviour I know of is in Box Jellyfish, which use simple visual contrast to avoid obstacles."

All jellyfish are sensitive to a variety of external factors such as light, orientation, water currents, temperature, and a variety of types of touch, so they're by no means as unsophisticated as you're trying to make out. It's notable that you avoid trying to deal with echinoderms, which like most animals with radial rather than bilateral symmetry, also lack cen

You are nothing but a hypocrit. We know that at the very early stages of "life" a human embryo is almost equal to others, such as the chimp or the pig, but even a chicken embryo is almost identical. You justify this by adding a bullshit constant to the equation, the human embryo has a "soul". This complete and utter bullshit "allows" you to isolate "humans" (I put humans in citation marks because "humans" severely differ genetically, up to 12% of the genome) entirely from animals and plants. This bullshit of yours prevents important research to develop safer and more advanced medical treatment. I don't want to be forced to leave my child fatherless one day just because you're a selfish asshole. So you know what? Go fuck yourself.

I'm sorrowful. Sorrowful because of earlier comments. Is it really big achievement to read short paper and then write review of "Brief Report"? Nevertheless slashPOTTERS! The idea is quite old. Thomson et.al. described this idea in this paper: http://www.sciencemag.org/cgi/content/abstract/318/5858/1917 . There are earlier, but this one is good one and representative too.

I suppose that questions about possible mechanism come from ignorance and laziness. Partially answer can be found here :http://images.cell.com/images/Edimages/Cell/IEPs/3661.pdf

Besides, I think that questions about capabilities of lay out the mixture of proteins can be answer in following way. If we try to analyze how DNA vectors work into cells, we can conclude, that they impact on some part of biochemical pathways. They of course don't impact directly but through interactions with some others molecules e.g: proteins. Because this relation is injection (in mathematical sense ) so we can conclude, that deep analysis of DNA role in generating iPSCs can deliver us hints which proteins should we use. The best mixture we get (if our criterion is simplicity of mixture), when we find proteins in bijection relation with DNA vectors. Of course it is not simple task, but without analysis of genetic process in generating iPSCs we will able only to shoot wild.

If someone is interested about this subject I recommend this papers:
+ http://www.cell.com/cell-stem-cell/retrieve/pii/S1934590908005250
+ http://www.ncbi.nlm.nih.gov/pubmed/17554338

There's only one real obstacle. Make it affordable.

And just what do you think you're going to do with it? TFA is a stupid, hype filled mess (as usual). The original article is here. The big deal is thus:

- Pluripotent stem cells MAY (big time maybe) be useful in a wide array of clinical applications.
- Embryonic stems cells are hard to obtain, have ethical issues to some folks.
- Fibroblasts (skin cells) are easy to obtain, not so ethically high strung and easy to grow.
- We've known for a couple of years that you can create what look to be stem cells by infecting fibroblasts using four (count'em only four) separate proteins. That's pretty amazing - the whole differentiation cascade is apparently controlled by a small number of discrete molecules.
- The problem is that to get those proteins inside the fibroblasts you have to use a (real) virus, which is interesting called a "Trojan" since it's "bringing in" foreigners. That is conceptually unappealing because the "stem cells" now have some viral garbage which may or may not interfere with experiments.
- The current research gets said proteins inside the cell using another clever "hack" - a small peptide (apparently derived from HIV infected cells) that allows the bigger proteins to sneak inside and do their magic.

- On first and second blush, the newly transformed stem cells look and act like Pleuripotent Embryonic Stem Cells (the real McCoy).
- But this remains to be seen, many a grant and paper are yet to come.

So don't get all wound up thinking you can inject this stuff into you and magically turn 16 again. Remember, you can only be young once.

But you can be immature forever.

I'm a biochem post-doc working in a molecular-microbiology lab. We're studying E.coli O157:H7 and attempting to inhibit intimin formation.

intimin is a protein on the surface of the cell membrane which allows the bacteria to adhere. no intimin and the bacteria stay in solution, therefore no more quorum sensing, no more bio-film and no infection! voila!

Sounds easy, right? Those little critters just won't cooperate though!

But, back to papers. At the institutions I've been at it's quantity first, quality 2nd, and brand-name distant 3rd. Quantity is easy. Quality is harder - it's best judged over time by the number of cites. If your peers cite your papers as the basis for their work, you're doing something right. Scientists are being rated by their citations now.

As for brand - no one really cares if you publish in Cell, Journal of Bacteriology, Molecular Microbiology or PLoS Pathogens. (unless, of course it's top-tier Science/Nature/PNAS, etc. any guess as to what percentage of submitted papers those top tiers represent?)

Why would you give your work away to some publisher so they can make a buck? What do you get out of it? You give them your paper. Signing the copyright over to them. You work for them for free, peer-reviewing papers so they can have a peer-reviewed journal. And then they make $$$ money selling them, restricting their audience, and give you nothing. That seems right to you? Just so you can say your insignificant little paper [>90% are] was published in XXX journal?

I don't care if I never make a major discovery, but if the guy/gal who "cures" EHEC cites my work on intimin formation my scientific dreams would have been fulfilled. I will have participated in what Newton described with "If I have seen further it is by standing on the shoulders of giants".

rho

http://download.cell.com/neuron/pdf/PIIS0896627308009586.pdf

There are the pics. Haven't had time to read through the text yet, but I did see 3 pixelated reconstructions next to the original image.

Not very good quality, but better than what we had before (nothing.)

Probably requires a subscription to get it. As most do on this site, feel free to complain about that, but realize it's not the researcher's fault. They did provide the pics. The journalists at Asahi and Yomuri didn't, but you're not reading real science papers if you're reading newspapers.

People read blurby summaries, which don't include the results, the full reasoning, methods, etc, and then act as if it's the fault of the researchers. It's absurd, that's neither the paper nor the direct work of the researchers, it's some non-scientist working for a news source. Read the actual paper, TFA in these cases are rarely any better than TFS.

http://download.cell.com/neuron/pdf/PIIS0896627308009586.pdf

There's the PDF. It does have the very pixelated images. I haven't had time to read through it.

As always, don't complain to me if you don't happen to have a subscription, and not having a subscription is no reason to act as if the results aren't real.

What? In 1997? You probably meant 2007, and your link says 2007, too. Still, this is not the first such work. The first pioneering work was not done by University of Wisconsin or by Harvard. It was first published by a research group in Kyote, Japan in 2006: http://www.cell.com/content/article/abstract?uid=PIIS0092867406009767 Everyone in the stem cell research know that these guys are very likely to get the Nobel!

For those with access to the journal Cell, you can view The Castilla, et al, paper online (this abstract should be available for all). The nature link in the summary goes to a write-up about the article, not the actual article itself.

Those with subscriptions to Cell can also get the full text, Full Text in PDF, and the Supplementary Data.

For those with access to the journal Cell, you can view The Castilla, et al, paper online (this abstract should be available for all). The nature link in the summary goes to a write-up about the article, not the actual article itself.

Those with subscriptions to Cell can also get the full text, Full Text in PDF, and the Supplementary Data.

For those with access to the journal Cell, you can view The Castilla, et al, paper online (this abstract should be available for all). The nature link in the summary goes to a write-up about the article, not the actual article itself.

Those with subscriptions to Cell can also get the full text, Full Text in PDF, and the Supplementary Data.

For those with access to the journal Cell, you can view The Castilla, et al, paper online (this abstract should be available for all). The nature link in the summary goes to a write-up about the article, not the actual article itself.

Those with subscriptions to Cell can also get the full text, Full Text in PDF, and the Supplementary Data.

For those with access to the journal Cell, you can view The Castilla, et al, paper online (this abstract should be available for all). The nature link in the summary goes to a write-up about the article, not the actual article itself.

Those with subscriptions to Cell can also get the full text, Full Text in PDF, and the Supplementary Data.

Real geeks read Cell (with pictures)

DOI: 10.1016/j.cell.2008.06.051

http://www.cell.com/content/article/fulltext?uid=PIIS0092867408008386

AMPK and PPARÎ Agonists Are Exercise Mimetics

The benefits of endurance exercise on general health make it desirable to identify orally active agents that would mimic or potentiate the effects of exercise to treat metabolic diseases. Although certain natural compounds, such as reseveratrol, have endurance-enhancing activities, their exact metabolic targets remain elusive. We therefore tested the effect of pathway-specific drugs on endurance capacities of mice in a treadmill running test. We found that PPARÎ/Î agonist and exercise training synergistically increase oxidative myofibers and running endurance in adult mice. Because training activates AMPK and PGC1α, we then tested whether the orally active AMPK agonist AICAR might be sufficient to overcome the exercise requirement. Unexpectedly, even in sedentary mice, 4 weeks of AICAR treatment alone induced metabolic genes and enhanced running endurance by 44%. These results demonstrate that AMPK-PPARÎ pathway can be targeted by orally active drugs to enhance training adaptation or even to increase endurance without exercise.

Firstly, this isn't Digg, can we please not link to blogs? The original paper from Cell is here: http://download.cell.com/pdfs/0092-8674/PIIS009286 7407007015.pdf.

Secondly, this is exciting news, but not exactly surprising. The differentiation of cells starts in the bone marrow, and there are biochemical signals that start that process. It's not surprising that some of these would be in bone marrow.

Finally, must these articles always make a point to imply that obesity is cause by some random genetic/biochemical "magic bullet," instead of eating poorly and not exercising? I understand that they need funding, and implying you may be able to "cure" obesity is a great way to get it. Even so, I think there's something rather disingenious about it.

http://www.cell.com/content/article/fulltext?uid=P IIS0092867404000315

Haven't we known about caspase cascades and mitochondria for several years... I'm pretty sure I learned about them in AP Biology five years ago.

I didn't say "scientists", I said "life science researchers". And I stand by what I said. The overwhelming majority of life science researchers have never heard of TeX, outside of some very small computational and theoretical niches. The premier molecular biology journal, for example, requests "Word, RTF, and TXT".

A variety of molecules in human blood have been implicated in the inhibition of HIV-1. However, it remained elusive which circulating natural compounds are most effective in controlling viral replication in vivo. To identify natural HIV-1 inhibitors we screened a comprehensive peptide library generated from human hemofiltrate. The most potent fraction contained a 20-residue peptide, designated VIRUS-INHIBITORY PEPTIDE (VIRIP), corresponding to the C-proximal region of 1-antitrypsin, the most abundant circulating serine protease inhibitor. We found that VIRIP inhibits a wide variety of HIV-1 strains including those resistant to current antiretroviral drugs. Further analysis demonstrated that VIRIP blocks HIV-1 entry by interacting with the gp41 fusion peptide and showed that a few amino acid changes increase its antiretroviral potency by two orders of magnitude. Thus, as a highly specific natural inhibitor of the HIV-1 gp41 fusion peptide, VIRIP may lead to the development of another class of antiretroviral drugs.

http://www.cell.com/content/article/abstract?uid=P IIS0092867407003285 - Discovery and Optimization of a Natural HIV-1 Entry Inhibitor Targeting the gp41 Fusion Peptide
Summary

A variety of molecules in human blood have been implicated in the inhibition of HIV-1. However, it remained elusive which circulating natural compounds are most effective in controlling viral replication in vivo. To identify natural HIV-1 inhibitors we screened a comprehensive peptide library generated from human hemofiltrate. The most potent fraction contained a 20-residue peptide, designated VIRUS-INHIBITORY PEPTIDE (VIRIP), corresponding to the C-proximal region of 1-antitrypsin, the most abundant circulating serine protease inhibitor. We found that VIRIP inhibits a wide variety of HIV-1 strains including those resistant to current antiretroviral drugs. Further analysis demonstrated that VIRIP blocks HIV-1 entry by interacting with the gp41 fusion peptide and showed that a few amino acid changes increase its antiretroviral potency by two orders of magnitude. Thus, as a highly specific natural inhibitor of the HIV-1 gp41 fusion peptide, VIRIP may lead to the development of another class of antiretroviral drugs.

Rather than just the abstract here is the full article text.

I encourage you to read the primary literature of the study: http://www.cell.com/content/article/fulltext?uid=P IIS0092867406014656&highlight=salter Then your opinion may or may not change, or may or may not have any credibility left. As a trained scientist, I think this is a very remarkable study, far more promising then the stop-gap measures we currently have for diabetes treatment. Let's not make opinions based on headlines.

The newspaper article is a not quite accurate either, although it has less hyperbole than the parent. What the study actually says is that it appears that the sensory nervous system is playing a role in the development and progression of diabetes. That is the "blockbuster", since it was thought to be an autoimmune disease.

If verified, it provides yet another avenue of investigation into diabetes control and possibly cure, but this is a first study. A lot of work needs to be done to go between this and a standard treatment.

Important? Yes. Break out the champagne and declare diabetes is cured? No.

I left out from the above comment:
The latest (2006) article at
http://www.cell.com/content/article/abstract?uid=P IIS0092867406014656
mentions The Jackson Laboratory, but that is not appear to be traded.

Yes, because using Google is so damn hard. Enter "Cell Journal" into Google. First link. The Article is available.

The article is in Cell, a highly respected journal. Here is the link to the published article, and the associated commentary (subscription required).

Commentary: http://www.cell.com/content/article/abstract?uid=P IIS0092867406015340
Article: http://www.cell.com/content/article/abstract?uid=P IIS0092867406014656

The article is in Cell, a highly respected journal. Here is the link to the published article, and the associated commentary (subscription required).

Commentary: http://www.cell.com/content/article/abstract?uid=P IIS0092867406015340
Article: http://www.cell.com/content/article/abstract?uid=P IIS0092867406014656

ok, ok, i'll do the work for you...

http://www.cell.com/content/article/abstract?uid=P IIS0092867406014656

the link to the PDF for the entire article is to the right of the page

How had this crap got itself published in Cell???

http://www.cell.com/content/article/abstract?uid=P IIS0092867402008188

I spot a trend here ;-)

The assumption that DNA exists solely to produce proteins is wrong. Current research suggests that DNA (via mRNA) has a direct role in memory formation in the brain. In fact, many genes have been identified whose role it is not to produce proteins, but serve as a mechanism in thought and memory formation and reinforcement. Considering that there may be many similar or identical functions in the brain with regards to thought and memory, intelligent organisms having multiple copies of these memory controlling genes is unsurprising.

here's a related study for you:
http://www.cell.com/content/article/abstract?uid=P IIS0092867405014042

To draw a software analogy:
Lets say the compiled binary + all configuration and data files of your program is DNA. There are parts of the of the program that define proteins and physical structures i.e. data files, string constants, etc. There are also parts that define the sequence of events from start to finish, growth, and change i.e. the instruction code that gets sent to the CPU for processing.

For DNA that controls memory and thought formation, we can think of this as meta-code or configuration files. These files dictate what parts of the instruction code get loaded, linked, and run and under what circumstances. This meta-code may not actually perform computation or build useful data (no growth, no respiration, no protein production), but it defines how the program (organism) operates.

e.g. One bit of code might load the appropriate vectorized FP library when there is hardware support. Or, biologically, one bit of DNA might make a person always remember technical information under normal circumstances.

On top of that the Cell Press journals have one of the more open policies of commercial high-profile journals where they open up free access to journal articles for everyone a year after they're published. Compare that to Nature or Science. . .

The transmissible agent causing canine transmissible venereal tumor (CTVT) is thought to be the tumor cell itself. To test this hypothesis, we analyzed genetic markers including major histocompatibility (MHC) genes, microsatellites, and mitochondrial DNA (mtDNA) in naturally occurring tumors and matched blood samples. In each case, the tumor is genetically distinct from its host. Moreover, tumors collected from 40 dogs in 5 continents are derived from a single neoplastic clone that has diverged into two subclades. Phylogenetic analyses indicate that CTVT most likely originated from a wolf or an East Asian breed of dog between 200 and 2500 years ago. Although CTVT is highly aneuploid, it has a remarkably stable genotype. During progressive growth, CTVT downmodulates MHC antigen expression. Our findings have implications for understanding genome instability in cancer, natural transplantation of allografts, and the capacity of a somatic cell to evolve into a transmissible parasite.

is here.

The last movie is the best.

There was actually an article on this a few days ago.

Original research paper in Cell: Environmental Enrichment Reduces Alpha-Beta Levels and Amyloid Deposition in Transgenic Mice
Summary in Cell: Exercise Your Amyloid

Article in Medical News Today

Quote: Mice that keep their brains and bodies busy in an "enriched" environment of chew toys, running wheels, and tunnels have lower levels of the peptides and brain plaques associated with Alzheimer's disease compared to mice raised in more sparse conditions, according to a new study in the 11 March issue of the journal Cell.

Levels of b-amyloid peptides, which clump together to form the brain "tangles" or plaques that are toxic to nerve cells in Alzheimer's disease, were significantly lower in the enriched mice, say Sangram Sisodia, of the University of Chicago, and colleagues. The enriched mice may have been better equipped than their less-stimulated counterparts to sweep these peptides out of the brain, according to the researchers' analysis of gene and enzyme expression in the animals.

"This goes back to the old idea of use it or lose it, that using your brain keeps it more active," Sisodia says. "It's more common sense than anything, but what we didn't previously appreciate is that it might affect the pathology that is characteristic of Alzheimer's disease." ...

The researchers also found intriguing clues that an active body, as well as an active brain, might be a key factor in reaping the benefits of an enriched environment. The most physically active of the mice in the elaborately furnished cages had the most dramatic reductions in amyloid peptides and deposits. At least among this small group of mouse workout devotees, "exercise appears to play a significant role in modulating amyloid deposition," Sisodia and colleagues write.

The researchers caution, however, that it will take more experiments with larger numbers of animals to determine exactly how enriched environments benefit mice, whether through increased physical activity, a boost in visual, social, and spatial stimuli that awaken the brain, or some combination of all of these factors.

Sisodia says exercise, along with any kind of mental activity from reading to doing the crossword puzzle, are probably the equivalent of chew toys and running wheels for humans. "It's all very important in keeping the mind active and potentially staving off effects of old age."

What works in a dish of cells is often an entirely different story in an entire organism. It will be exciting when their virus manages to, say, keep an SIV-infected monkey alive for five years post-infection.

Seven years ago, a custom rhabdovirus (rabies) for selectively killing HIV-infected cells had my biotechnolgy professor all excited, but nobody's heard from them for a while since it didn't work in whole organisms.

(Why yes, I _am_ a molecular biologist....)