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After 15+ years of this "ice 9" business I'm still waiting for results that in any way meet Koch's Postulates.

OK, this one will cover a lot of ground. Weber P et al. Cell-free formation of misfolded prion protein with authentic prion infectivity. Proc. Natl. Acad. Sci USA 2006 October 24; 103(43): 15818–15823. It's open-access, so no excuses about being stuck behind a paywall.

Making claims that biochemists working on prions "don't like to get dirty" is both insulting and disingenuous. Animal models are, in fact, used here to demonstrate that purified PrPsc (misfolded prion protein) is infectious in live hosts, in addition to triggering misfolding in vitro. No one uses farm animals because they're large, expensive, and there's no compelling reason to incur that cost when simpler model animals (here, hamsters) will do.

why not entertain the notion that this is a slow virus and that the symptomatic misfolded protein is a mere phenotype, possibly detrimental, but not causal

Well, because the linked paper was able to amplify the infective population of PrPsc in a cell-free system, which would not be conducive to the amplification of a virus.

I understand the appeal of an underdog hypothesis, but unless you can present a better argument that isn't comprised of ad hominems, vague conspiracy theories, and a smattering of scientific claims answered by 5-year-old literature, I'm not convinced.

It was tried out 17 years ago in Endeavour with chicken eggs and guess what happened...

They all died :-(

Just count the sons of female astronauts which birth date is prior to landing + nine months, but I guess they are none.

Sure they do in many cases, especially as analgesics.

The grossest thing about meat in the grocery store is all the chemicals they have to spray the meat down with to kill all the bad stuff and disease picked up from the animal from living in such poor conditions.

Well that's a load of shit. Please, do tell us which horrible horrible "chemicals" are sprayed on these poor diseased carcases, exactly. Maybe you could also link to a peer-reviewed study showing the significantly higher incidence of disease amongst animals raised using different methods. Go ahead, I'll wait.

I can easily imagine without resorting to peer-reviewed journal articles that there are "conditions" that could result in higher and lower incidence of disease among animals. After all, we know from our own experience as animals that our own living conditions greatly affect the incidence of disease in our populations. Consider typhoid, a disease that all but disappears in areas with modern sanitation.

I see no reason to believe that animals raised in poor sanitary conditions, would be sicklier than animals raised in good sanitary conditions. Do you really need a cite? Really? You were just trolling with that one.

As for chemicals used in cleaning carcasses -- besides water and steam -- here's an abstract from an article in the "Journal of Food Protection". Your wait is over!

Reports on the microbiological effects of decontaminating treatments routinely applied to carcasses at beef packing plants indicate that washing before skinning may reduce the numbers of enteric bacteria transferred from the hide to meat. Washing skinned carcasses and/or dressed sides can reduce the numbers of aerobes and Escherichia coli by about 1 log unit, and pasteurizing sides with steam or hot water can reduce their numbers by > 1 or > 2 log units, respectively. Spraying with 2% lactic acid, 2% acetic acid, or 200 ppm of peroxyacetic acid can reduce the numbers of aerobes and E. coli by about 1 log, but such treatments can be ineffective if solutions are applied in inadequate quantities or to meat surfaces that are wet after washing. Trimming and vacuum cleaning with or without spraying with hot water may be largely ineffective for improving the microbiological conditions of carcasses. When contamination of meat during carcass dressing is well controlled and carcasses are subjected to effective decontaminating treatments, the numbers of E. coli on dressed carcasses can be [less than] 1 CFU/ 1,000 cm2. However, meat can be recontaminated during carcass breaking with E. coli from detritus that persists in fixed and personal equipment. The adoption at all packing plants of the carcass-dressing procedures and decontaminating treatments used at some plants to obtain carcasses that meet a very high microbiological standard should be encouraged, and means for limiting recontamination of product during carcass breaking and for decontaminating trimmings and other beef products should be considered.

There are 10 more articles found with the search "cleaning beef carcasses" at pubmed.

And that was just the first suggestion from Google.

The grossest thing about meat in the grocery store is all the chemicals they have to spray the meat down with to kill all the bad stuff and disease picked up from the animal from living in such poor conditions.

Well that's a load of shit. Please, do tell us which horrible horrible "chemicals" are sprayed on these poor diseased carcases, exactly. Maybe you could also link to a peer-reviewed study showing the significantly higher incidence of disease amongst animals raised using different methods. Go ahead, I'll wait.

I can easily imagine without resorting to peer-reviewed journal articles that there are "conditions" that could result in higher and lower incidence of disease among animals. After all, we know from our own experience as animals that our own living conditions greatly affect the incidence of disease in our populations. Consider typhoid, a disease that all but disappears in areas with modern sanitation.

I see no reason to believe that animals raised in poor sanitary conditions, would be sicklier than animals raised in good sanitary conditions. Do you really need a cite? Really? You were just trolling with that one.

As for chemicals used in cleaning carcasses -- besides water and steam -- here's an abstract from an article in the "Journal of Food Protection". Your wait is over!

Reports on the microbiological effects of decontaminating treatments routinely applied to carcasses at beef packing plants indicate that washing before skinning may reduce the numbers of enteric bacteria transferred from the hide to meat. Washing skinned carcasses and/or dressed sides can reduce the numbers of aerobes and Escherichia coli by about 1 log unit, and pasteurizing sides with steam or hot water can reduce their numbers by > 1 or > 2 log units, respectively. Spraying with 2% lactic acid, 2% acetic acid, or 200 ppm of peroxyacetic acid can reduce the numbers of aerobes and E. coli by about 1 log, but such treatments can be ineffective if solutions are applied in inadequate quantities or to meat surfaces that are wet after washing. Trimming and vacuum cleaning with or without spraying with hot water may be largely ineffective for improving the microbiological conditions of carcasses. When contamination of meat during carcass dressing is well controlled and carcasses are subjected to effective decontaminating treatments, the numbers of E. coli on dressed carcasses can be [less than] 1 CFU/ 1,000 cm2. However, meat can be recontaminated during carcass breaking with E. coli from detritus that persists in fixed and personal equipment. The adoption at all packing plants of the carcass-dressing procedures and decontaminating treatments used at some plants to obtain carcasses that meet a very high microbiological standard should be encouraged, and means for limiting recontamination of product during carcass breaking and for decontaminating trimmings and other beef products should be considered.

There are 10 more articles found with the search "cleaning beef carcasses" at pubmed.

And that was just the first suggestion from Google.

Basically what you feed is what you get in weight gain...

You raise a good point on feed. Cattle are currently fed Corn for a variety of reasons. However, this is not a cow's natural source of food, and it makes them produce more methane than they would naturally.

What would happen if the bug farmer's changed the bug's diet to something more economical? Would their methane production change?

Addictive Potential

Long-term marijuana abuse can lead to addiction; that is, compulsive drug seeking and abuse despite the known harmful effects upon functioning in the context of family, school, work, and recreational activities. Estimates from research suggest that about 9 percent of users become addicted to marijuana; this number increases among those who start young (to about 17 percent) and among daily users (25-50 percent).

Long-term marijuana abusers trying to quit report withdrawal symptoms including: irritability, sleeplessness, decreased appetite, anxiety, and drug craving, all of which can make it difficult to remain abstinent. These symptoms begin within about 1 day following abstinence, peak at 2-3 days, and subside within 1 or 2 weeks following drug cessation.3

Physical Dependence

Two decades ago, addiction medicine doctors and counselors believed that the difference between substance abuse and substance dependence was whether tolerance and withdrawal were present. Now it is known that, although tolerance or withdrawal may occur in individuals with addiction, the condition of addiction can exist without any sign of tolerance or withdrawal. Still, a common question of interest is, does marijuana produce physical dependence (that is, tolerance or withdrawal)?

By the twenty-first century, the answers to these questions are clear. Tolerance does develop to THC (the active chemical in marijuana). Moreover, withdrawal definitely occurs in some users. The effects of this withdrawal are generally the opposite of the effects of intoxication: anxiety and insomnia instead of relaxation; loss of appetite rather than hunger; excessive salivation instead of dry mouth; and also decreased pulse, irritability, and sometimes tremor. People who have used marijuana as a way to control underlying anger may also experience irritability, increased mood swings, and even an increase in aggressive behavior, as symptoms of withdrawal.

Long-Time Marijuana Use Linked to Psychosis in Young Adults

Respiratory Effects of Marijuana and Tobacco Use in a U.S. Sample

Emphysema linked to smoking marijuana

Addictive Potential

Long-term marijuana abuse can lead to addiction; that is, compulsive drug seeking and abuse despite the known harmful effects upon functioning in the context of family, school, work, and recreational activities. Estimates from research suggest that about 9 percent of users become addicted to marijuana; this number increases among those who start young (to about 17 percent) and among daily users (25-50 percent).

Long-term marijuana abusers trying to quit report withdrawal symptoms including: irritability, sleeplessness, decreased appetite, anxiety, and drug craving, all of which can make it difficult to remain abstinent. These symptoms begin within about 1 day following abstinence, peak at 2-3 days, and subside within 1 or 2 weeks following drug cessation.3

Physical Dependence

Two decades ago, addiction medicine doctors and counselors believed that the difference between substance abuse and substance dependence was whether tolerance and withdrawal were present. Now it is known that, although tolerance or withdrawal may occur in individuals with addiction, the condition of addiction can exist without any sign of tolerance or withdrawal. Still, a common question of interest is, does marijuana produce physical dependence (that is, tolerance or withdrawal)?

By the twenty-first century, the answers to these questions are clear. Tolerance does develop to THC (the active chemical in marijuana). Moreover, withdrawal definitely occurs in some users. The effects of this withdrawal are generally the opposite of the effects of intoxication: anxiety and insomnia instead of relaxation; loss of appetite rather than hunger; excessive salivation instead of dry mouth; and also decreased pulse, irritability, and sometimes tremor. People who have used marijuana as a way to control underlying anger may also experience irritability, increased mood swings, and even an increase in aggressive behavior, as symptoms of withdrawal.

Long-Time Marijuana Use Linked to Psychosis in Young Adults

Respiratory Effects of Marijuana and Tobacco Use in a U.S. Sample

Emphysema linked to smoking marijuana

Since your writing appears to indicate you have a buzz on right now, and probably can't search for anything, I'll help you get started:

Respiratory Effects of Marijuana and Tobacco Use in a U.S. Sample

I never said that preservatives were not necessary, but that there was no explanation given as to, "why thimerosal (the mercury presevative used in vaccines) was used as opposed to the raft of other potential presevatives." See that last part?

You didn't seem to do much investigation at all apparently: "Unlike other vaccine preservatives used at the time, thiomersal does not reduce the potency of the vaccines that it protects." reference indicated

So, they used thiomersal, because it is: a) necessary to use preservatives, and b) the only preservative that would not reduce the potency of the vaccine.

Except for the Kleck study, most studies show that self-defense is not common. A more typical study found:

During the study interval (12 months in Memphis, 18 months in Seattle, and Galveston) 626 shootings occurred in or around a residence. This total included 54 unintentional shootings, 118 attempted or completed suicides, and 438 assaults/homicides. Thirteen shootings were legally justifiable or an act of self-defense, including three that involved law enforcement officers acting in the line of duty. For every time a gun in the home was used in a self-defense or legally justifiable shooting, there were four unintentional shootings, seven criminal assaults or homicides, and 11 attempted or completed suicides.

Short-term memory impairment is a common side-effect of the drug.

Hallucinations, by definition, are perceptual experiences that aren't caused by an external stimulus. They too are associated with brain activity in the appropriate sensory areas. For example, see this paper by Ffytche et al. (1998), which describes activity in various parts of visual cortex during visual hallucinations. So even if you do detect activity in some sensory area, you wouldn't be able to rule out an internally-generated cause. Detecting activity would merely confirm that the perceiver's brain is acting as if it is perceiving something...

Is it reasonable to expect that now that there would be a sizable sample size of "non-immunized" kids, that a study to compare the rates of autism between the two groups will be done?

Already done in 2002. There was a study done in Denmark (where there are comprehensive medical records for the whole population) that showed no link between MMR vaccination and autism rates.

A Danish study of more than half a million children showed no link between measles, mumps, and rubella (MMR) vaccination and autism.
In a commentary accompanying the study, which was published in the , Dr Edward Campion, senior deputy editor, wrote, “This careful and convincing study shows that there is no association between autism and MMR vaccination.”

Lead author Dr Kreesten Meldgaard Madsen, an epidemiologist and expert on infectious diseases at the Danish Epidemiology Science Centre in Aarhus, told the BMJ that the study showed that the risk of autism was similar in children who were vaccinated and children who were not.

The study reviewed records of 537303 children born in Denmark between January 1991 and December 1998, representing almost 100% of children born in that period. Of these children 440655 had been vaccinated.* Records were retrieved from three sources: the unique identification number assigned to each child at birth; MMR vaccination data reported to the National Board of Health by general practitioners, who give all MMR vaccinations and are reimbursed for their reports; and diagnoses of autism recorded in the Danish Psychiatric Central Registry. Only specialists in child psychiatry diagnose autism and related conditions.

Full story...

*My emphasis.

Inconvenient facts like this will not convince the Jenny McCarthys and Jim Careys of this world though.

For most vaccination requirements, anyone born prior to January 1, 1957, does not need to provide proof of immunity for measles, mumps, and rubella. This date was selected because the majority of people born prior to 1957 developed immunity against measles and mumps from natural infection due to widespread disease.

The modern death rate from measles in under 0.1%, but in poor countries may be as high as 10% ( http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1712354/ ). This is the rate for people who actually get the disease and is similar to the death rate from seasonal flu. So, the old guy, born before 1957, with all of his friends having had measles, should have lost somewhere around 1% of his childhood friends to measles. I'm not surprised he can't think of anyone who _died_ of measles.

It's also striking that (developed world) people born after 1970 can't generally think of anyone who's even _had_ measles, let alone died from it. What a great change in a decade.

Typically, as long as you have 85% or so vaccinated

Uhm, you're numbers are off a bit. At least for measles, it takes more like 95% (see http://www.ncbi.nlm.nih.gov/pubmed/20392713). Unless you have better, peer-reviewed data?

As long as most people are vaccinated you aren't likely to contract the disease, but if you are vaccinated it puts you at risk for side effects.

Also, CDC reported several hundred vaccine reported deaths in the last 10 years. I personally would rather my child have a small risk of allergic reaction or a mild illness than die. Particularly if the mild illness is part of keeping the group as a whole well, but the death my own fault.

Why don't you look on pubmed, the largest database of research articles, and take a look? Hint: the pro-science side of the debate actually understands what goes on when you administer a vaccination; vaccination does not mean 100% immunity. Also those outbreaks occur where clusters of people don't get their kids vaccinated, and in those outbreaks the unvaccinated kids are disproportionally overrepresented compared to their proportion of the population at large.

http://www.ncbi.nlm.nih.gov/pubmed/16322148?ordinalpos=1&itool=PPMCLayout.PPMCAppController.PPMCArticlePage.PPMCPubmedRA&linkpos=3

Though his statement is misleading at best. Out of 9 cases (in a school of over 600), 7 of them were vaccinated (1 with a single dose, 6 with both doses) and 2 were not vaccinated. The 7 vaccinated cases falls within the typical vaccine failure rate.

I recall having a little discussion about this a week or so ago on /., at the time of the bee research by 8-year olds, in which I linked to this PLoS paper. It's from 2005, not exactly new.

I don't think it's a problem with the research in itself, but the demand to get things published or funded by demonstrating statistical significance. Most researchers aren't statisticians, but know that demonstrating a p-value of less than 0.05 (at least in biomedical research) is good enough to convince most publishers and funders. Test 20 different things, and chances are than one of those things will pass this significance threshold. That chance effect will end up getting published and the rest will be left behind as useless work. I find the bit about "gold-standard" research three pages into TFA to be particularly telling:

In 2005, Ioannidis published an article... that looked at the forty-nine most cited clinical-research studies in three major medical journals.... the data Ioannidis found were disturbing: of the thirty-four claims that had been subject to replication, forty-one per cent had either been directly contradicted or had their effect sizes significantly downgraded.

Note it mentions "of the claims that had been subject to replication". If you look at the abstract of that paper, only 20 (44%) of the most cited studies were replicated, and 11 (24%) remained largely unchallenged.

But wait, there's more:

Claims from highly cited observational studies persist and continue to be supported in the medical literature despite strong contradictory evidence from randomized trials.

I don't think this is as much of a problem in the fields of mathematics and physics, because they are more likely to understand the statistics involved in demonstrating that something is a real effect. I have heard that physicists only accept p-value cutoffs that are approaching the planck constant in magnitude, which would be somewhat harder to fudge.

I recall having a little discussion about this a week or so ago on /., at the time of the bee research by 8-year olds, in which I linked to this PLoS paper. It's from 2005, not exactly new.

I don't think it's a problem with the research in itself, but the demand to get things published or funded by demonstrating statistical significance. Most researchers aren't statisticians, but know that demonstrating a p-value of less than 0.05 (at least in biomedical research) is good enough to convince most publishers and funders. Test 20 different things, and chances are than one of those things will pass this significance threshold. That chance effect will end up getting published and the rest will be left behind as useless work. I find the bit about "gold-standard" research three pages into TFA to be particularly telling:

In 2005, Ioannidis published an article... that looked at the forty-nine most cited clinical-research studies in three major medical journals.... the data Ioannidis found were disturbing: of the thirty-four claims that had been subject to replication, forty-one per cent had either been directly contradicted or had their effect sizes significantly downgraded.

Note it mentions "of the claims that had been subject to replication". If you look at the abstract of that paper, only 20 (44%) of the most cited studies were replicated, and 11 (24%) remained largely unchallenged.

But wait, there's more:

Claims from highly cited observational studies persist and continue to be supported in the medical literature despite strong contradictory evidence from randomized trials.

I don't think this is as much of a problem in the fields of mathematics and physics, because they are more likely to understand the statistics involved in demonstrating that something is a real effect. I have heard that physicists only accept p-value cutoffs that are approaching the planck constant in magnitude, which would be somewhat harder to fudge.

http://www.ncbi.nlm.nih.gov/pubmed/1262518

Title: "Jehovah's Witnesses and human tissue donation."

Abstract: "Because of their religious beliefs members of the Jehovah's Witnesses sect do not permit human tissue donation, not even such a routine and life-saving procedure as blood transfusion. A group of 30 adult Jehovah's Witnesses was compared with groups of donors and nondonors on a variety of personality measures. Donor status is associated with a well-integrated body image and acceptance of mortality, while nondonor status correlates with a less-well-integrated body image, concern about body integrity, and anxiety about death. However, while Jehovah's Witnesses vigorously oppose human tissue donation they appear to do so on strong religious grounds rather than because of personal anxiety and thus are dissimilar to non-donors at large."

Sure seems like another church could be slightly less strenuous on the same grounds, perhaps by adding the word "involuntary"... anyone else thinks the Pastafarians should add this doctrine to their cannon? Just Saying...

-- Terry

I see you didn't even bother to read the line you quoted, I said nothing about increased neural activity. Nor did I say anything about physical lifespan. Oh well, morons happen.

A medical explanation? Sure, no problem. The brain has two mechanisms for storing new information - neurogenesis (growth of new brain cells) and new connections between those brain cells.

Forming new brain cells is a little tricky, but you don't need to. The neurological fact is that the brain grows excess brain cells before birth. The unused ones die off, leaving what is actually used. There is then a second surge in brain cell numbers at around age 12, which peaks at 18-20. The die-back begins 25-30.

This is hard-and-fast medical science. It is simply not in dispute.

Now, it is known that learning increases the number of neural connections, and that learning new languages increases the neural connections significantly. Learning from different language families - as it's the most complex task involving learning the most - can reasonably be taken as adding the most neural connections.

"Ah! But wait!" Some might say. "This only proves that there's more connections, not connections between more brain cells."

True, so you have to add in further studies. This one and this one show that intensive learning connects more brain cells.

The more you learn before the brain starts to die back, the more room for connections you will have and the more possible paths you will end up with. This is simple mathematics.

Ok so far?

Good.

The brain's capacity to self-repair is impressive (as demonstrated by Scott Adams' regained ability to speak, for example) but it is finite. The more brain cells you have and the more neural connections you have, the more of those can be damaged without seriously impacting the performance of the whole. Thus, aging effects will be mitigated. However, the above studies also suggest that the rate of naturally-occurring cell death from age is also reduced.

Health problems? Sure, but I said nothing about health problems. I stated, quite clearly, "functional lifespan" - the lifespan the brain is going to be capable of functioning at some given level of capacity. This should be considered in relation to the mean functional lifespan of the brain of mono-linguists in the same environment.

(Thus, a polyglot in the construction industry should have the mental speed and agility necessary to work in such conditions for longer than a monoglot, where the extended ability is roughly a linear function of the languages learned.)

In short, if you want to critique me, be VERY VERY sure of your facts because I am going to rip any pseudo-scientific bullshit to shreds.

I see you didn't even bother to read the line you quoted, I said nothing about increased neural activity. Nor did I say anything about physical lifespan. Oh well, morons happen.

A medical explanation? Sure, no problem. The brain has two mechanisms for storing new information - neurogenesis (growth of new brain cells) and new connections between those brain cells.

Forming new brain cells is a little tricky, but you don't need to. The neurological fact is that the brain grows excess brain cells before birth. The unused ones die off, leaving what is actually used. There is then a second surge in brain cell numbers at around age 12, which peaks at 18-20. The die-back begins 25-30.

This is hard-and-fast medical science. It is simply not in dispute.

Now, it is known that learning increases the number of neural connections, and that learning new languages increases the neural connections significantly. Learning from different language families - as it's the most complex task involving learning the most - can reasonably be taken as adding the most neural connections.

"Ah! But wait!" Some might say. "This only proves that there's more connections, not connections between more brain cells."

True, so you have to add in further studies. This one and this one show that intensive learning connects more brain cells.

The more you learn before the brain starts to die back, the more room for connections you will have and the more possible paths you will end up with. This is simple mathematics.

Ok so far?

Good.

The brain's capacity to self-repair is impressive (as demonstrated by Scott Adams' regained ability to speak, for example) but it is finite. The more brain cells you have and the more neural connections you have, the more of those can be damaged without seriously impacting the performance of the whole. Thus, aging effects will be mitigated. However, the above studies also suggest that the rate of naturally-occurring cell death from age is also reduced.

Health problems? Sure, but I said nothing about health problems. I stated, quite clearly, "functional lifespan" - the lifespan the brain is going to be capable of functioning at some given level of capacity. This should be considered in relation to the mean functional lifespan of the brain of mono-linguists in the same environment.

(Thus, a polyglot in the construction industry should have the mental speed and agility necessary to work in such conditions for longer than a monoglot, where the extended ability is roughly a linear function of the languages learned.)

In short, if you want to critique me, be VERY VERY sure of your facts because I am going to rip any pseudo-scientific bullshit to shreds.

"work" is ambiguous and slightly deceptive. What we should say is there is a "reported effect". That is different (from my perspective) as having a clinical effect.

Hróbjartsson & Gøtzsche did an interesting meta-analysis of studies with both a placebo and no-treatment arm. For binary outcomes (except pain) there was no significant difference and for continuous outcomes and binary pain outcomes there was a difference but it increased inversely with sample size. They postulate that what people call the "placebo effect" is really just a form of reporting bias. People have been "treated" or have gone though the motions of treatment and as a result they change their expectations.

I mean, what is more likely some mysterious force which crosses every clinical boundary...or that people are (unintentionally) fudging things a bit.

After reading the slashdot summary, I got to wondering - do Placebos actually "work" or is it simply that the patients would get better all by themselves (immune system and other self-healing mechanisms in the body)? So, I did a few seconds of googling "placebo vs no treatment", and came upon a paper online at the NIH website:

http://www.ncbi.nlm.nih.gov/pubmed/12535498

The author of that paper concludes, "There was no evidence that placebo interventions in general have clinically important effects."

If the healing happens a certain percentage of the time regardless of whether treatment is even administred, then it makes perfect sense that placebo would work that same percentage of the time, even if people didn't believe they were being treated - e.g. "belief" has nothing to do with recovery - that is, it's very possible, and that NIH paper appears to confirm the hypothesis, that with "placebo effect", the conscious mind plays no role in the improvements witnessed.

There are a number of experiments which explore both nanopore scaling and eletrode interference. The majority of them are under grants at http://projectreporter.nih.gov/reporter.cfm. These and other future projects are summarized in plain text at Dna Sequencing

Navigating that query form at nih is impossible!

There are a number of experiments which explore both nanopore scaling and eletrode interference. The majority of them are under grants at http://projectreporter.nih.gov/reporter.cfm. These and other future projects are summarized in plain text at Dna Sequencing

'...the entire genome is only 850,000,000 bytes which is 810.6MB'

That's about right - the reference assembly from UCSC is 778Mb in their standard .2bit format. That's just a single sequence for each autosomal chromosome plus one each of X and Y, though - you'll need to allow about double that to store your full dipoid genome, so better buy a 2Gb flash drive. On the other hand, if you take the reference sequence as a given and only store the differences between it and yours, you only need about 4Mb!:

http://www.ncbi.nlm.nih.gov/pubmed/18996942

But raw sequence data is a different matter. To call each base confidently everything has to be sequenced multiple times (it's normal to go for something like 40x coverage on an Illumina machine). And you'll probably have to deal with the files as uncompressed ascii text (or gzip/bz2 at best). When you start analysing the data, you'll need a lot more space to store the alignments to the reference sequence, and you'll need some reasonable computing power to do the processing (which may well take longer than generating the data).

They have been show to behave in a manor similar to asbestos when inserted into mouse tissue http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2783215. However, when trying to determine the dangers of using a given material in a product there are two factors that need to be considered. One is how large of an expose is dangerous. Water will kill you if you drink enough of it. The second other is mechanisms of exposure. If you smashed the glass in your window and ate it would shred your stomach lining and probably kill you. Does this mean that we should ban the use of glass?

The reason asbestos was so bad is they put it in insulation, which when disturbed released a lot asbestos into the air. From there it could be inhaled. You can design a product using carbon nanotubes in such a way the the risk of exposure minimized. This would include steps such as embedding the carbon nanotubes in a polymer in a fashion such that significant quantities of carbon nanotubes will not be released into the air and coating the surface of the product with a material to will prevent significant quantiles from being absorbed though the skin while in contact.

There are two reasons that carbon nanotubes have not shown up in commercial products. The first is price. If I am recalling correctly carbon nanotubes cost about 100 dollars per gram. For comparison the price of gold in about 30 dollars per gram. The second is that actually carbon nanotube composites have so far had properties far worse than classic composites models would predict. Two reason for this are that carbon nanotubes are hard to evenly disperses within the filler material and the bonding between the filler material and the carbon nanotubes has been more problematic than it has with larger diameter fibers such as carbon fiber. That being said carbon nanotubes still have the potential to be a hugely useful material for many possible applications; however, there are still many basic research questions about producing and using carbon nanotubes that need to be resolved.

But only completely for type 2: http://www.youtube.com/watch?v=46_GInjBeQU
See also: http://www.drfuhrman.com/disease/diabetes.aspx

Type 1 diabetics still need to take insulin, but can take less and have less complications. So, this idea from the article might eventually help them.

From that link: "John ... was a 22 year old college graduate with Type 1 diabetes since the age of 6. He was five foot, eight inches tall and weighed 190 pounds. He was taking a total of 70 units of insulin daily. He was referred to my office by his family physician as he was having swings in his glucose levels, too high at times and at other times dangerously low. He also wanted to learn more about nutrition to improve his health and reduce his future risks from having diabetes. I was impressed by his intelligence and desire to change his eating habits to better his health. We spent lots of time discussing the typical problems that befall most diabetics, and I explained to him that using 70 units of insulin a day was part of the problem. I explained that if he follows my recommended diet-style he will stabilize his weight at about 145 pounds and he will only require about 30 units of insulin a day. With this lower level of insulin, to mimic the amount of insulin a non-diabetic makes in the pancreas, he can have a life without the typical health issues that befall diabetics. We cut his nighttime insulin dose down by ten units and his mealtime insulin from 10 to 6 as he began the diet. Over the next two weeks we gradually tapered his insulin and found that he only needed 20 units of Lantus insulin at bedtime and 4 units before each meal for a total of 32 units a day. Almost immediately, with my dietary recommendations, his sugars were running in the favorable range, and he no longer experienced dangerous drops in his blood sugar. He had lost 13 pounds over the first month and by month three weighed 167, a loss of 23 pounds. He was excited about what he had learned and was more hopeful about his life while living with his diabetes. I am convinced, that with the Eat To Live or Eat For Health diet-style, those with Type 1 diabetes can have a long and disease-free life. I feel it is imperative that all Type 1 diabetics learn about this life, saving approach."

Key there for type 1 diabetics is reducing complications, even if they still take diabetes.

Type 1 diabetes may also be related to vitamin D deficiency in utero and early life.
http://www.ncbi.nlm.nih.gov/pubmed/18846317
http://www.google.com/custom?q=diabetes&sitesearch=vitamindcouncil.org

If you have type 2 diabetes, you can most likely, within weeks under Dr. Fuhrman's plan, be throwing your insulin away forever (at least, based on what he writes). I know you may find this hard to believe. The key idea there is to lose weight to reduce insulin resistance, and to eliminate refined carbs to reduce insulin needs, and to improve your body's general health with more phytonutrients, and so bring the need for insulin within the remaining capacity of your body. In most cases of type 2 diabetes this should be enough to eliminate the need for any medications. Even if you remained on medications, the risk of complications would go way down and the quality of your life would go way up.

See also Raw For Thirty (though Dr. Fuhrman's approach is more comprehensive and not all raw for some good reasons):
http://www.rawfor30days.com/

Some people think they have type 1 diabetes because they have been misdiagnosed and are really type 2 and presumably 100% curable. I guess the opposite may be true, too, sadly. In any case, you never know for sure till you try.

I am following the Eat to Live plan for other reasons (though not

Yeah, what bknabe said: http://stemcells.nih.gov/info/basics/basics10.asp [nih.gov]. Score another one for adult stem cells.

Sorry to be a stickler over terms, but "adult stem cell" and "induced pluripotent stem cells" are two different things. An adult stem cell is a stem cell from the adult (or child) body which can effectively be used as is. These generally have a narrower range of fates. You can take a blood stem cell and it will produce blood cells. It will not produce neurons, but you don't have to change it's epigenetics to get it to produce blood.

iPS on the other hand are cells which don't need to be stem cells initially, but have to be epigenetically "reset" to produce anything. To do this, you need to manipulate it a bit to make it more like an embryonic stem cell. The upside is that it can produce, say, spinal cord neurons, and you avoid host rejection since you can use a patient's own cells. The downside is that the manipulations are very low efficiency and the risk of producing cancer is likely increased.

Two different things. This is a "score" for iPS, not adult stem cells. I guess it's not too important if you're more concerned with "They're not harvested from embryos" than accuracy, but there is a real difference.

Yeah, what bknabe said: http://stemcells.nih.gov/info/basics/basics10.asp. Score another one for adult stem cells.

You are far too generous -- there was a comment on this paper in the next issue of the journal entitled Tai's formula is the trapezoidal rule. There is nothing complicated or clever about it.

Tai's article was printed in February of 1994. An author comment printed in the October 1994 issue is titled "Tai's formula is the trapezoidal rule." I don't have full text access to either, but the title of the followup is not encouraging.

'Yeah, but a human has ~3 billion base pairs. IANACS, but with 2 bits per base, so one byte represents 4 bases, so it's roughly equivalent to 750 megabytes. That's pretty impressive compression to shrink to 50 megs (which I agree, is a lot of data).'

Indeed. The 2-bit encoded human genome available from UCSC runs to 778Mb, or a conventional gzipped ASCII file is 905Mb. Better compression is an active area of research. Depending on the complexity of the input sequence and the compression algorithm, various values in the 1-2 bits/base pair range have been quoted, see e.g.:

http://fabrice.lefessant.net/papers/cpm2005.pdf

But that still leaves you far short of Kurzweil's supposed compression ratio, unless you allow this sort of cheating:

http://www.ncbi.nlm.nih.gov/pubmed/18996942

This trick relies on comparison to a known standard reference sequence, and therefore doesn't say anything about the information content of the genome in general (so it's no good for Kurzweil's argument).

'Then again, if you skim the "junk DNA" (which may or may not really be junk), you can shrink it quite a bit'

If you include only protein-coding genes and discard the rest as 'junk', you can get to around Kurzweil's number in uncompressed ASCII. But that really is cheating. There's lots going on outside the proteome:

http://scienceblogs.com/transcript/2007/02/dinner_with_the_transcription.php

So you have to deal with all 3 billion bp.

http://www.ncbi.nlm.nih.gov/pubmed/5636472

Follow up study on this topic (triclosan in toothpaste) in 2005:
http://www.ncbi.nlm.nih.gov/pubmed/16208383

Points still stand.

Triclosan covered toothbrushes? At one time science showed that triclosan reduces plaque. And what causes plaque in the first place? Bacteria! Don't put the blame solely on marketing. Be informed!
http://www.ncbi.nlm.nih.gov/pubmed/2638181

On the contrary, the vast majority of human cancers have telomerase (are "immortal"), perhaps what you're thinking of is the ability to grow in culture, which is a relatively rarer phenomenon (HeLa cell line!) but nowadays can be artificially induced. This makes sense because a cancer's rapid growth rate would be unsustainable in the long term without some way of getting around telomere loss. The rapid division combined with most cancer's predisposition to mutation results in natural selection for these specific kinds of mutations - the first cell to express telomerase, for example, will out-compete his shorter-lived brothers in the long run, so inevitably all cancers wind up circumventing the telomere issue in one way or another. If you've got access, you can read this nice review article: http://www.ncbi.nlm.nih.gov/pubmed/9282118

The only possible reason you've heard

absolutely no science to back that statement up.

is either because you are deaf, dumb, or lazy. The research is pretty clear. Flying causes skin cancer, but has little to no effect on the incidence of other kinds of cancer. Thirty seconds of google-fu brings up:

http://www.cancerhelp.org.uk/about-cancer/cancer-questions/airline-staff-and-cancer

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC124549/

http://oem.bmj.com/content/57/3/175.abstract

What you describe is a significant component of what The Human Microbiome Project is about.

Right, and battery acid is really good at curing the common cold.

I dunno where you're getting this info, but no, bullets certainly do not "sterilize" anything. One of the leading causes of death historically has been infection. We're better at dealing with it today, but infections still occur on a regular basis:

"A gunshot is never sutured closed as the infection rate is very high. Bullets drag clothing into the wound and along the bullet track. Since clothing is of course not sterile, the wound is prone to infection if closed. Open wounds almost never get infected."
http://www.tacticalmedicalpacks.com/files/Combat_Tactics_Trauma_article.pdf

"We have presented a series of 120 consecutive operative cases of penetrating wounds of the abdomen-72 gunshot wounds and 48 stab wounds. The majority of patients were in the 18 to 40 age group. The infection rate was 22% for gunshot wounds and 4.8% for knife wounds."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2609419/pdf/jnma00480-0069.pdf

Hell-loooooo!

Anyone thinking in there?

Mars is already post-apocalyptic, times a factor of a million!

And it's tens of millions of miles away, on a good day.

If we're worried about catastrophe, we should be looking for ways to prevent it for everyone's sake, not just helping the super-wealthy and astronautically psychotic avoid it.

obligatory
695

Yes! And the additional health-benefit of inhaling loose, blowing nano-particles - and the subsequent introduction to the pulmonary systems of city-dwellers - is surely the cincher on this!

I'm guessing you either failed at your own logic or at reading my post. GP said: "Making X illegal would not fix the problem, these people already have X illegally." In his post, X = guns. My post was pointing out the foolishness of such an argument by replacing X with murder. In other words, just because criminals already have guns, doesn't mean making guns illegal wouldn't be better for society.

Yes I know, you're trying to imply because the reverse case in an analogy is not necessarily true, that the original argument is not true. That's pretty badly broken logic.

I'll break it down for you: GP made a statement, that since people already have guns, making guns illegal doesn't fix the problem. That is, we have some action or state of being (having guns), and laws making that action or state of being illegal does no good. My counter (stated sarcastically) was that making murder (an action) illegal _does_ do good. In other words, we have an example of where making an action or state of being illegal does some good. You may not like the analogy, but the logic is sound: laws do good for society.

Honest question: are you saying that our laws do no good? Or that our laws against murder do no good? Is that where I'm "failing" at logic?

It's actually fairly sound logic to imply that making it illegal to say, own butcher knives, won't decrease the number of people killed in muggings, since there are plenty of alternative weapons and people carrying butcher knives for purposes of mugging are already breaking several laws, so causing them to break one more is unlikely to work as a deterrent. The same holds true for firearms.

Making it illegal to own butcher knives almost certainly would reduce the number of deaths by butcher knife. And it is also sound to say that it is easier to kill with a gun than with a knife. And it is sound to say that by making it more difficult to kill people, less people will be killed.

Regarding the rest of your post, we've obviously read different studies (excepting the ones correlating drug decriminalization with a better society), but we can at least argue the points on the data and not on our own personal experience.

I'd love for you to provide a citation. Let me caution you, however, 90% of the studies I see people cite suffer from a logical misstatement of the problem characterized by the term "gun crime". I'm sure if you think about it and you have taken any courses on informal logic, this error will be fairly obvious.

We're talking about whether a gun makes you safer. I've already provided a citation, above. Here's another on suicide: http://www.ncbi.nlm.nih.gov/pubmed/17426563.

Quoting:

CONCLUSION: Household firearm ownership levels are strongly associated with higher rates of suicide, consistent with the hypothesis that the availability of lethal means increases the rate of completed suicide.

The data I've seen (and provided) supports the hypothesis that less gun ownership means more safety.

One would think that any sensible journalist would be cautious throwing titles like "Central dogma of genetics maybe not so central" with the only scientific publication being a conference lecture.

That's what I thought after reading this ./ post. But then I found (type: "Cheung VG[au] AND Philadelphia" into the search bar)) that the main author had some respectable publications on the subject.

Even with respectability of the authors of the original publication established, the sensationalist title in Science News is nowhere near the modest conclusions of the authors.

Actually all Crick stated in his "Central Dogma" is that information can flow from NA to NA and NA to P, but not from P to P or P to NA, information being defined as the precise sequence of bases of AA resides. The linear sequence of DNA > RNA > protein was not part of Crick's "dogma", it just seems to have virally infected it and spread by endless replication.

I reproduced the exact quote elsewhere on the thread but forgot to include its author. See "On Protein Synthesis" by F. H. C Crick.

To throw a further spanner in the works, a large proportion of non-genetic DNA (i.e. the stuff that doesn't get eventually converted into proteins) has functional aspects — it is transcribed into RNA and then used directly for cellular regulation (see here).

The original poster was correct. Glaucoma causes high intraocular pressure, which if untreated will lead to vision loss and blindness. Medicated eyedrops will keep the intraocular pressure low and prevent blindness. Check it out.

Can anyone find the original journal article? From a fairly quick PubMed search, James' group last published on TRIM21 back in 2008. There have been a few papers on TRIM21 in 2010, but they're not from James' institution and they don't share any authors with James' 2008 paper.

Or is this being reported before the paper has been published? Do we know that it has even been properly reviewed?

This is really cool if it's true and it's relevant to my research, so I'd love to see the original paper.