Archive for January, 2008

Target Earth

January 31, 2008

Earth

One hundred years ago, a large meteoroid or comet exploded in the sky over Tunguska, Siberia. We don’t know that much about it: Estimates on size vary from 30 to 1,200 meters in diameter, and estimates on the force of the blast are in a range of 3 to 30 megatons of TNT (”about 1,000 times more powerful than the bomb dropped on Hiroshima”). But we do know that the explosion leveled trees over 2,150 square kilometers (830 square miles)…

Tunguska Event
Photograph from the Soviet Academy of Science 1927 expedition led by Leonid Kulik. Public domain.

To coincide with this anniversary, the Planetary Society has launched the Target Earth project, a year-long focus on “on Near Earth Objects (NEOs) and the hazards that marauding space-rocks pose to our planet.”

Target Earth encompasses The Planetary Society’s three-pronged approach to NEO research: funding researchers who discover and track asteroids, advocating greater NEO research funding by the government, and helping spur the development of possible ways to avert disaster should a potentially dangerous asteroid be discovered.

You can learn more about the Gene Shoemaker NEO Grants here. Some quick facts:

(more…)

Promising Anti-Radiation Drug Based on Carbon Nanotubes

January 31, 2008

Radioactive

The Defense Advanced Research Projects Agency (DARPA) gave a $540,000 grant to researchers from Rice University to do a fast-tracked 9-month study on a new anti-radiation drug based on carbon nanotubes:

“More than half of those who suffer acute radiation injury die within 30 days, not from the initial radioactive particles themselves but from the devastation they cause in the immune system, the gastrointestinal tract and other parts of the body,” said James Tour, Rice’s Chao Professor of Chemistry, director of Rice’s Carbon Nanotechnology Laboratory (CNL) and principal investigator on the grant. “Ideally, we’d like to develop a drug that can be administered within 12 hours of exposure and prevent deaths from what are currently fatal exposure doses of ionizing radiation.” [...]

The new study was commissioned after preliminary tests found the drug was greater than 5,000 times more effective at reducing the effects of acute radiation injury than the most effective drugs currently available. [...]

The drug is based on single-walled carbon nanotubes, hollow cylinders of pure carbon that are about as wide as a strand of DNA. To form NTH, Rice scientists coat nanotubes with two common food preservatives — the antioxidant compounds butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) — and derivatives of those compounds.

An interesting side benefit of the drug might be that it could also potentially help cancer patients who are undergoing radiation treatment.

Source: Feds fund study of drug that may prevent radiation injury

See also: Creating a Technological Immune System

This piece was cross-posted on the Lifeboat Foundation Blog.

Ode to my CPU

January 30, 2008

Athlon 64, 1.8ghz, 3000+, 90nm

This is a picture of the CPU that has been in my desktop computer for the past 4 years. It is an AMD Athlon 64 3000+. One “Windsor” 90nm core running at 1.8 GHz, fitting on socket 939 with dual channel memory.

There’s no problem with it. It’s still working, and has always been dependable, running cooly even when I pushed it to 100% usage with distributed computing projects. But I’ve replaced it with an Athlon 64 X2 3600+ (2 cores running at 2 GHz). These are so cheap now, and I figured it would be a good way to do more data crunching inexpensively. I know that my computer will keep being used for a few years - if not by me, but my parents or someone else - so more than doubling the amount of scientific work it can do makes a difference.

I don’t get sentimental about objects. I don’t collect stuff. But holding that CPU in my hand made me realize how fantastic our technology is, and how many great things it allows us to do. Had I been born in a non-networked world without inexpensive computers, there is so much things I wouldn’t know, so many people I never would have connected with, so many books unread, so much music unheard. I wouldn’t have the job I have now, and you wouldn’t be reading this.

I certainly wouldn’t be the same person…

So this is my homage to my CPU.

Athlon 64, 1.8ghz, 3000+, 90nm

Curing Alzheimer’s Disease

January 29, 2008

Brain MRI

My paternal grandmother gradually lost her memory up to the point she was basically as functional as a newborn baby. According to the National Institute on Aging, about 5% of men and women between the age of 65 and 74 have Alzheimer’s disease, and about half of those 85 and older may have the disease.

In his book Ending Aging, biogerontologist Aubrey de Grey explains that Alzheimer’s is a disease related to aging, caused by damage that accumulates with time and, at a certain age, reaches a threshold that turns it into a pathology. The cause is most likely the accretion of beta-amyloids in the brain, a type of mis-folded protein.

The implications are that we’ll all get Alzheimer’s if something else doesn’t kill us first, and as our life expectancy rises, the risk goes up.

So this disease is one of the challenges standing in the way of curing aging (and reducing human suffering in general), and defeating it is something that we could all benefit from. This is why I encourage you to donate to the Methuselah Foundation and join a distributed computing project that works on computational protein design like Rosetta@Home (join my team here), or protein folding (and mis-folding) like Folding@Home.

But don’t despair! There’s some good news:

Arun Ghosh, at right, and Xiaoming Xu
Arun Ghosh, at right, and Xiaoming Xu. Credit: Purdue University.

A molecule designed by a Purdue University researcher to stop the debilitating symptoms of Alzheimer’s disease has been shown in its first phase of clinical trials to be safe and to reduce biomarkers for the disease.

CoMentis, the pharmaceutical company developing the drug, announced on Jan. 7 completion of its Phase 1 study of a treatment based on the molecule. Results from the study indicate that the treatment is safe and well tolerated. [...]

The molecule, called a beta-secretase inhibitor, prevents the first step in a chain of events that leads to amyloid plaque formation in the brain. This plaque formation creates fibrous clumps of toxic proteins that are believed to cause the devastating symptoms of Alzheimer’s.

The study of 48 healthy volunteers showed dose-related reduction in plasma amyloid beta, a protein believed to be a key biomarker of Alzheimer’s. Results showed a single dose of the drug produced a greater than 60 percent reduction of the biomarker. Subjects received one of six different doses or a placebo, and the study measured levels of the therapeutic drug and levels of the biomarker in the bloodstream.

CoMentis plans to begin a phase II clinical study of the drug, oral CTS-21166, in Alzheimer’s patients in 2008.

It’s too early to tell if this specific drug will work, but the goal certainly is to clean up the damage in the brain before it leads to Alzheimer’s. A cure for people who already have the disease would be fantastic, but the real goal is to avoid getting it in the first place.

Sources:

Some Progress on Universal Influenza Vaccine

January 29, 2008

Influenza Vaccine

According to ScienceDaily:

The British-American biotech company Acambis reports the successful conclusion of Phase I trials of the universal flu vaccine in humans. The universal influenza vaccine has been pioneered by researchers from VIB and Ghent University. This vaccine is intended to provide protection against all ‘A’ strains of the virus that causes human influenza, including pandemic strains. Therefore, this vaccine will not need to be renewed annually.

What would make this new vaccine different from the ones already available is that it would target M2e, a conserved region of influenza “A” strains. Since that part doesn’t constantly mutate and about 2/3 of seasonal epidemics and all pandemics are due to type “A” strains, it could be a very efficient weapon against repeats of the “Spanish Flu” (1918-1919) that killed at least 50 million people worldwide. Only the future will tell if phase II and III trials are successful.

You can learn more about the Lifeboat Foundation BioShield program here.

This piece was cross-posted here on the Lifeboat Foundation Blog.

Near Earth Objects: We Can’t Beat the Odds Forever

January 27, 2008

Asteroid 2007 TU24
Orbit diagram of near Earth object 2007 TU24. Nasa JPL, original here.

Mark your calendars. On January 29th, 2008, the near Earth object (NEO) 2007 TU24 will pay us a visit. Thankfully, it’s just passing by and not stopping. It will zip by at 0.0038 Astronomical Units from our planet, which is about 1.4 lunar distances. That’s 568,472 kilometers, or 353,232 miles. In astronomical terms, that’s the other cowboy grazing your head with a bullet.

I’ve written more extensively about Near Earth Objects a few months ago. Since then, the distributed computing project Orbit@home which wants to monitor asteroids has been funded by Nasa. The latest news is that active development of the project will start in March 2008. Can’t wait to let my CPUs loose on that one. In the meantime, here are other worthy projects that I encourage you to check out.

So what if we detect a rock and do the math, find out that it has us in the cross hair. What then? Well, there are many theories on how to deflect inbound space rock. But theories are not enough. We need to make this happen sooner rather than later, because as 2007 TU24 reminds us, we can’t beat the odds forever.

Update: 2007 TU24 is “estimated at between 150 and 600 meters in diameter — about 500 feet to 1,900 feet, or the size of a football field, at 360 feet, to the size of Chicago’s 110-story Sears Tower, at 1,454 feet”.

Sources:

Creating a Technological Immune System

January 27, 2008

Cell Phones
Photo by Prateek Karandikar. GFDL and Creative Common (BY-SA) licenses.

Using already existing networks to create inexpensive and vast early-detection systems is simply brilliant.

Researchers at Purdue University are working with the state of Indiana to develop a system that would use a network of cell phones to detect and track radiation to help prevent terrorist attacks with radiological “dirty bombs” and nuclear weapons.

Such a system could blanket the nation with millions of cell phones equipped with radiation sensors able to detect even light residues of radioactive material. Because cell phones already contain global positioning locators, the network of phones would serve as a tracking system, said physics professor Ephraim Fischbach. [...]

Tiny solid-state radiation sensors are commercially available. The detection system would require additional circuitry and would not add significant bulk to portable electronic products, Fischbach said. [...]

“It’s impossible to completely shield a weapon’s radioactive material without making the device too heavy to transport,” Jenkins said.

Of course, participation would need to be voluntary for it to be ethical, but I’m sure that there would be more than enough volunteers to make it work.

Think of the possibilities of such a vast network of sensors: How about detecting certain chemicals? With the right technology, it could even detect biological and viral threats. I know they’re already working on sensors that can monitor air quality. What else can we think of?

Sources:

See also:

The Individuals-as-Groups Fallacy

January 25, 2008

Acropolis
Acropolis of Athens. Photo G. Larson. Public domain.

Democracy: It is the best system we know to take group decisions and it has a very strong and positive ‘brand’. But is it possible that we use it too much? By that I mean that there are many things that we decide democratically that actually don’t require group decisions to achieve the best results — there are many areas of life where individuals would be best positioned to decide what is best for themselves, but others force their decisions on them.

Humans have a tendency to see groups everywhere, and democracy can compound the downsides of that flaw. Liberals, conservatives, people of various religious beliefs, atheists, whites, latinos, blacks, arabs, jews, Americans, Chinese, Frenchmen, environmentalists, rich, poor, middle-class, urban, rural, majority, minorities, etc. Within that framework, people start to actually identify with their group and to dislike others, especially those they are in a power-struggle with. It’s a rational reaction because within a democratic system, some groups hold power over others and nobody wants a group they dislike to impose decisions on them. No, they’d rather impose their truth on others. This allows power-hungry politicians to play identify politics and try to have groups identify with them and thus overlook things that they would never accept on an individual basis. It’s all very tribal-like (you can also observe that phenomenon in sports).

When people stop seeing individuals, it can quickly lead to dehumanization and polarization (and we know where these can lead). They see caricatures and don’t take the time to get to know people who are in groups that they dislike: as soon as a label comes up, their minds shut down and whatever their reasons (based on reality or not) for disliking that group, they project them on the individual. “Surely if I hate jews, I’ll hate that jew.” “Surely if Frenchmen are annoying, I’ll be annoyed by that Frenchman.” Then confirmation bias kicks in…

Opposite factions rarely make the effort to really understand the positions/culture/etc of the other side(s) (liberals read liberal blogs, conservatives read conservative blogs), which means that few people change their minds and even fewer pick rational positions based on the best available information that can be gathered from all sides.

Free yourself from these shackles. Force yourself to see people as individuals, because that’s what they are. And so are you, and I’m sure you wouldn’t want others to look at you as some insignificant part of a larger over-simplistic monolith.

Irrationality Can Screw Up Your Life

January 24, 2008

As if we needed more evidence that rationality is a good thing, it now seems like irrationality is not just something that will lead you to have crazy beliefs and not understand how the world works; it can also kill you (among other things).

Scott Beaulier and Bryan Caplan argue in a paper titled Behavioral Economics and Perverse Effects of the Welfare State that the traditional explanation about crime being more attractive to the poor because their legal options to improve their situation are limited is unsatisfactory.

It might seem intuitive that more poor people commit crimes because they are trying to get out of poverty, but evidence shows that most crimes are not very lucrative.

Their theory?

What’s my alternative? Crime is just one of many, many “social pathologies” that are over-represented among the poor: alcoholism, drug abuse, smoking, obesity, illegitimacy, etc. None of these are good escape routes from poverty. So instead of trying to explain why “poverty causes crime” or “poverty causes obesity,” it makes sense to look for common causes of poverty and social pathologies.

Like what? In a paper just accepted by Kyklos, Scott Beaulier and I point to a simple candidate: irrationality. People who have biased beliefs about practical matters, and/or exercise poor impulse control, are likely to screw up their lives across the board. So it’s hardly surprising that poverty and self-destructive behavior go hand in hand. Rather than being a natural response to poverty, a lot of crime can be seen as objectively self-destructive behavior that happens to have an unusually large amount of collateral damage. (link)

This seems consistent with anecdotal evidence that poor but educated people aren’t as likely to suffer from these social pathologies (and by educated I most certainly am not talking only about formal schooling).

It’s not about how much is in your wallet, but how much is in your head. So get smart (you can if you have a growth mindset).

Incubating a New Project Pt.2

January 22, 2008

After thinking about this some more, I’ve come to the conclusion that it wouldn’t work. Maybe with some other book, but not with Molecular Biology of the Cell.

A.J. Jacobs could read 100 pages of the Britannica and then pick 5 interesting entries to write about, add some anecdotes about how he used his new knowledge in his daily life and voilà. That wouldn’t work with a textbook, I’d end up summarizing almost everything because it’s all inter-linked and that’s not something I want to do.

I’ll keep an eye open for another book that could be turned into a book diary, and I’m certain I’ll find a few cool stand-alone parts in Molecular Biology of the Cell that I can write about here, but for now I’m putting this project on ice.

Incubating a New Project

January 22, 2008

The Know-It-All, by A.J. Jacobs

I’m reading The Know-It-All, A.J. Jacobs’ book detailing his experience reading the whole 2002 edition of the Encyclopeadia Britannica, and it gave me an idea. Maybe I could document my journey through a difficult book too. The first that comes to mind is Molecular Biology of the Cell, a technical but fascinating and well-written molecular biology textbook. I want to better understand how life works, and it seems like a good place to start.

I don’t think I could make it as entertaining as Jacobs’ book, but it might motivate some people to learn some biology in the same way that the Know-It-All makes me want to pick up an encyclopedia.

This project needs more thought before I commit to it. Molecular Biology of the Cell is an intimidating book, all 1,268 pages of it… Far from Britannica’s 34,000 pages, but hey, this is hard science! Figuring out a structure wouldn’t be quite as straightforward as mixing up historical trivia and personal anecdotes the way Jacobs does. Maybe I just won’t find a way to make it work — Encyclopedias offer bite-sized info while textbooks are more linear and constantly build on top of what came before, making it hard to skip over or isolate parts.

Pros: Even if I can’t make it all the way through, I’m sure I’d get something out of it, if only better retention of what I read.

Cons: I’m not exactly good at sticking to reading plans. My interests tend to be all over the place and go through phases (I’ll read a book on economics, then on WWII German generals, then on neuroscience, etc). But even if I read other books in parallels and sometimes pause because I’m too busy with other things, this could be a long-term, open-ended project.

To be continued…

Meditations on a Cell

January 17, 2008

Escherichia coli
Escherichia coli - Scanning Electron Microscopy. Public domain image.

The K-12 strain of E. coli, the best studied prokaryotic (meaning: without a nucleus — cells that have one, such as animals and plants, are in the eukaryote category) bacteria, has a genome that contains 4,639,221 nucleotide pairs.

These 4.6 million nucleotide pairs, which are contained in a single circular molecule of DNA that floats inside the plasma membrane of the bacteria (remember, no nucleus) can code about 4,300 different kinds of proteins (the tools and building blocks used by life).

Proteins are made from amino acids (there are 20 kinds). It takes 3 nucleotide pairs to code one amino acid; since there are 4 “letters” in DNA, T,A,G,C, you get 4 x 4 x 4 = 64 possibilities with 3 pairs, so some triplets code for the same amino acids. The code for each protein, depending on the organism and how it is expressed, can produce more than one variant of a protein. For example, humans have genes to code about 24,000 proteins, but our bodies can contain up to a million different variants.

To complicate things further, different strains of E. coli can be very different from each other. Some can contain hundreds of genes that are absent from others, and two strains can have as little as 50% of genetic material in common. Some have a flagella and are mobile while others are not, some can cause serious illness in their host (they usually colonize the human digestive system within 40 hours of birth, via food and water) and some are fairly benign. That high variability in genetic makeup within a single species can be explained in good part by the non-sexual reproduction of E. coli.

So all of these 4.6 million DNA base pairs, and these 4,300+ proteins, are working to create life within a relatively simple single cell organism that is less than one micrometer - one millionth of a meter - thick and not much more than two micrometers long. Even the smallest and simplest forms of life are incredibly complex and endlessly fascinating.

Now think about how mind-boggling our human bodies are (3.2 billion DNA base pairs, though not all of them gene-coding).

Biology is the new frontier.

In the Mail: A.I. & Neuroscience Books

January 14, 2008

Is Apathy a Disease?

January 9, 2008

Here is the abstract of a Harvard University study titled “Age-Related Changes in Simulation of Future Events” published in the January 2008 issue of Psychological Science:

Episodic memory enables individuals to recollect past events as well as imagine possible future scenarios. Although the episodic specificity of past events declines as people grow older, it is unknown whether the same is true for future events. In an adapted version of the Autobiographical Interview, young and older participants generated past and future events. Transcriptions were segmented into distinct details that were classified as either internal (episodic) or external. Older adults generated fewer internal details than younger adults for past events, a result replicating previous findings; more important, we show that this deficit extends to future events. Furthermore, the number of internal details and the number of external details both showed correlations between past and future events. Finally, the number of internal details generated by older adults correlated with their relational memory abilities, a finding consistent with the constructive-episodic-simulation hypothesis, which holds that simulation of future episodes requires a system that can flexibly recombine details from past events into novel scenarios.

I wish I had access to the whole study, but I don’t.

Still, unless I’m interpreting the abstract and this article wrong, it seem like the damage caused to memory functions by aging could make it harder for us to project ourselves into the future and generate possible scenarios for ourselves.

We all know that aging can be a terrible thing because of all the aging-related diseases that it brings (some people are working on that problem), but if on top of that it reduces our ability to think ourselves into the future, it will diminish our ability to care about it.

Maybe the movie cliché with the old guy telling the young one about how he “used to have dreams, used to think constantly about the future, but not anymore” isn’t just a cynical line but also a biological condition. Apathy is a disease? I don’t want to read too much into the Havard study, but this could explain many things.

One more reason - as if we needed more - to do our best to find ways to repair the damage of aging.

Discussion About War & Empire

January 3, 2008

Two weeks ago, Antiwar.com received a letter from a non-commissioned officer in the U.S. Marine Corps wondering what motivated our behavior. [...]

What follows, with his permission and with his name and rank omitted, is our discussion

You can find the whole discussion about war & empire here. It is surprisingly civil and informative. Highly recommended.

More Methuselah Foundation Good News

January 2, 2008

I’m happy to report that December 2007 year-end donations to fund the Methuselah Foundation’s Strategies for Engineered Negligible Senescence (SENS) research program succeeded in matching two consecutive $25,000 matching grants from Michael Cooper and Doug Arends. Many thanks to all the donors who helped to make this possible!

There’s more to come, however. Looking to the year ahead, and plans for expansion into new branches of SENS research, Foundation supporter Ryan Scott has set up a $100,000 matching fund for all research donations made in 2008. The same rules apply as for this past December: donations are first matched 100% by Ryan’s fund, and then that total is matched again at 50% by Peter Thiel’s $3 million matching fund. That means that all your SENS research donations will be tripled - a $100 donation becomes $300 for new research into longevity medicine.

Jump on in! These are the early years in a steep growth curve - and it’s up to all of us to help make that statement true. Donations to help bring about a future of greater health and longevity can be made at the Methuselah Foundation website, where you can also learn more about how funds are spent and the results achieved to date.

Be generous. Invest in something that could have hugely beneficial returns for all of humanity, including yourself.

See also: The Most Important Thing That Happened In 2007 at Fight Aging.

Update: The Economist has an article about the fight against aging and SENS.

To better understand what the Methuselah Foundation is about, check out this Aubrey de Grey speech. There’s a longer speech he gave at Google here. You can also read Aubrey de Grey’s book.

Also on this blog: