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Motorcycle helmets actually offer good protection, while bicycle helmets don't. For any impact over about 10 mph, they are not going to signifcantly reduce the peak accelerations your brain experiences (it's your brain sloshing that does the damage). I guess they can prevent lacerations, but that's about it. Helmet advocates always quote a study from the 1980s (funded by helmet manufacturers) that showed an 84% reduction in brain injuries, but other work has not borne this out. (example)

Wearing a helmet is applying a different standard to risk than we do in many other situations. Cycling is actually slightly safer per mile than walking, yet we don't make peds wear helmets. Just the same, we could make drivers wear helmets just like race car drivers do. That would actually prevent a huge number of deaths. But we don't. So why are cyclists singled out to wear the safety yarmulkes?

As an additional point, helment laws are actually terrible for cycling safety. After Australia made helmets mandatory, cycling went down 1/3 overnight. Fewer cyclists means drivers are less likely to expect them. In addition, there is evidence that cyclists wearing helments engage in riskier behavior as a form of risk-compensation.

> There are several viruses known to trigger the autoimmune response

Still significant. Do a search for the *bovine* enterovirus and diabetes. In the alternative medicine world, cows milk has been linked to diabetes ever since I can remember. A quick google shows this link has now been proven:

http://www.ncbi.nlm.nih.gov/pubmed/21922634

Interaction of enterovirus infection and cow's milk-based formula nutrition in type 1 diabetes-associated autoimmunity.

Source

        Immunogenetics Laboratory, University of Turku, Turku, Finland. johanna.lempainen@utu.fi

Abstract

BACKGROUND:

        Enteral virus infections and early introduction of cow's milk (CM)-based formula are among the suggested triggers of type 1 diabetes (T1D)-associated autoimmunity, although studies on their role have remained contradictory. Here, we aimed to analyse whether interactions between these factors might clarify the controversies.

MATERIALS:

        The study population comprised 107 subjects developing positivity for at least two T1D-associated autoantibodies and 446 control subjects from the Finnish diabetes prediction and prevention cohort. Enterovirus, rotavirus, adenovirus, respiratory syncytial virus and bovine insulin-binding antibodies were analysed from prospective serum samples at 3-24 months of age. Data on infant cow's milk exposure were available for 472 subjects: 251 subjects were exposed to cow's milk before 3 months of age and 221 subjects later in infancy.

RESULTS:

        Signs of an enterovirus infection by 12 months of age were associated with the appearance of autoimmunity among children who were exposed to cow's milk before 3 months of age. Cox regression analysis revealed a combined effect of enterovirus infection and early cow's milk exposure for the development of ICA and any of the biochemically defined autoantibodies (p=0.001), of IAA (p=0.002), GADA (p=0.001) and IA-2A (p=0.013).

CONCLUSIONS:

        The effect of enterovirus infection on the appearance of T1D-associated autoimmunity seems to be modified by exposure to cow's milk in early infancy suggesting an interaction between these factors. Moreover, these results provide an explanation for the controversial findings obtained when analysing the effect of any single one of these factors on the appearance of T1D-associated autoimmunity.

        Copyright © 2011 John Wiley & Sons, Ltd.

it sounds legitimate.

I review stuff like this for a living. This does look like a legitimate, promising study.

The guy has done a lot of research. http://www.ncbi.nlm.nih.gov/pubmed/?term=Hy%C3%B6ty%2C+Heikki%5BAuthor+-+Full%5D

TFA doesn't say what the virus is, but I guess that it's group B coxsackievirus 1. https://en.wikipedia.org/wiki/Coxsackie_B_virus#Diabetes that Hyöty was working on.

That said, it's a mouse study. I always used to say, "Mice, humans, what's the difference? We're all mammals, right?"

Then a researcher at Rockefeller University clued me in. "Humans are not big mice."

As the saying goes, "We've cured cancer in mice a million times."

It's great to model a disease in mice. But the diabetes type I they model in mice might not be the same as type I diabetes in humans. Probably for every 10 mouse studies, 1 holds up in humans. And for every 10 human studies, 1 turns out to be actually useful against the disease.

But hey, this is immunology. When it comes down to what causes a disease like diabetes type I, nobody really knows, so 1 in 100 is pretty good odds.

If you have 100 researchers working on it, you've got a pretty good chance that somebody will get it.

Diabetes type I is an autoimmune disease. You get exposed to a trigger, your immune system goes after the trigger, but it also starts attacking other things. In diabetes type I, it attacks the beta cells of the pancreas, which produce insulin. https://en.wikipedia.org/wiki/Diabetes_Type_I The trigger might be a virus, or it might be something else. Hyöty thinks it's a virus, in fact group B coxsackievirus 1. If he can prove that it is a virus and he's identified it (in humans, not just mice), he'll be doing pretty good.

And if Hyöty can come up with a vaccine that will prevent coxsackievirus infection in humans, we can give it to kids and they'll never get diabetes type I. That will be great. I hope it works.

”We know that this vaccine is effective in mice,” noted Hyöty. ”It is important to test it in people, so that we can be sure that the vaccine prevents diabetes.

That's the important qualification. If he's ready to go to test it in humans, that's pretty good. But he's still got a long way to go. And a lot of vaccines don't make it.

Taking the vaccine through a clinical trial would cost some 700 million euros. Some funding is in place from the United States and from Europe, but more is required.

Oh, give him the money. We've wasted E700 million on a lot of stupider things that you could probably think of.

If this vaccine is promising, then the big pharmaceutical companies will probably spot him E700 million for clinical trials (although that does seem a bit high). If it really does prevent type I diabetes, it should be a successful vaccine.

P2RX7 was all the hype back in January. Here's a blog entry on it... Or the paper abstract for the more technically inclined (pay-wall for paper)...

If people are interested, I think there is some more info in English concerning the earlier Tampere research here (for free)...

Sometimes it's hard to predict what is going to work in bio-science just by seeing the techno-press response. Although polio is caused by an Enterovirus, so is the common cold (the variety caused by a Rhinovirus). Generally you get Enterovirus infections orally. Some Enteroviruses can eventually enter the bloodstream and infect other organs.

Apparently, the Tampere study looked at the small-bowel mucosal biopsies of 120 patients and did a PCR technique to assess if there was likely a Enterovirus infection. 74% of people with type 1 diabetes tested positive, compared with 29% of the non-diabetic ones. On that basis they conclude that a persistent Enterovirus infection in the small-bowel might eventually spread to the pancreas where the on-going immune response might destroy the insulin producing cells leading to diabetes...

So, I wasn't totally impressed after reading that paper, but you never know...

Has anyone noticed that they now describe Man Made Global warming, which nobody uses anymore to describe climate change based on man made contribution, or that is, to initiate a world wide carbon tax, is now generic Climate Change?

The term "climate change" has been there from the beginning as evinced by a paper published in 1970 by George Benton titled "Carbon Dioxide and its Role in Climate Change". I believe the term was used at least as far back as the 1950's but I'm too lazy to track down a cite.

Bad article: most of the aspects discussed were first done ~10 years ago by Peter Schultz: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1299037/

http://en.wikipedia.org/wiki/Heptavalent_botulism_antitoxin
http://www.infantbotulism.org/general/babybig.php
http://www.ncbi.nlm.nih.gov/pubmed/21918119
http://www.cidrap.umn.edu/news-perspective/2006/02/antitoxin-infant-botulism-slashes-hospital-stays

The lab that discovered the new strain of botulism is a test center for infant poop. The drugs are terribly expensive so when a baby is suspected of having infant botulism, the hospital sends a sample that gets tested. If it's tested positive, the baby is given the antitoxin.

Seriously, use a web search. Not that hard.

40km is still only about 25 miles, which is well within that single horse's range. Interestingly enough, such a race already exists, and though it is usually won by a horse, humans have won before - and would likely win more often if the horse's maintenance times were counted in addition to the actual travel time.

Spurred on by this discussion*, I looked around a bit more, and I found an interesting article considering how humans can eventually outrun most other animals, complete with references.

* Pun intended. I'm terrible.

We're there, but it's not cheap and there are a lot of limitations. The shapes of the ribosome and its buddies are important for correct folding in many proteins.

Sorry, being lazy. Here is a nice recent overview:

Plausibility and evidence: the case of homeopathy.

Link to the abstract in some sort of fourth tier journal

Sorry, that abstract is garbage. They looked at a bunch of homeopathic studies and found 'evidence of an effect'. Without careful statistical analysis, that's just ... nothing. They even point out that most of the studies are garbage. I don't think that review would pass screening in any sort of reputable journal.

I'd like to see a single, statistically valid, study that does show an real effect of homeopathy. It's certainly possible to do.

If all clinical trials were viewed with such a critical eye as those supporting homeopathic treatment many fewer drugs would be approved.

The FDA actually approves very few drugs. It's Congressionally forced mandate is to prove the drugs 'safe' and 'effective', the latter meaning statistically equivalent to another drug or statistically better than a placebo arm.

So we have drugs that are 2% better than the old ones. While that may be statistically correct, it's not clinically meaningful - so we get lots of 'me too' drugs with clever advertising campaigns. OK, fine, what about safety? The new FDA requirements are crazy-strict. There are a number of older, grandfathered drugs that would never pass muster today. The FDA institutionally has gone full out on safety. That's a valid approach, but it leaves promising but potentially dangerous drugs unavailable. There is no real right or wrong here, just shades of gray.

But a homeopathic drug would never pass the efficacy portion of the testing since they've never demonstrated even statistically valid improvements over placebo.

In short, it's possible to show efficacy of a homeopathic drug using standard Double Blind Placebo Controlled Randomized Clinical Trials (DBPCRCT in the parlance). But no one really has, just vague handwaving.

There are studies that prove spices such as turmeric. . .

You mean (A HREF="http://www.ncbi.nlm.nih.gov/pubmed/23723666">one study which had 3 patients who were given turmeric capsules. This one study didn't prove anything. It only suggested there is some kind of link between properties in turmeric and the somewhat mitigated effects of Alzheimer's.

Further, it's not tumeric per se but curcumin, the source of turmeric, which seems to have the effect.

Teach your child to focus on their own health.

If I had children, I would but the government has said my health doesn't matter. What matters is your neighbors health which is why I'm forced to hand over my money to smokers, the obese, alcoholics and drug users who never have to change their ways.

Which seems to indicate that there is some basis for comparability between the two, even if they are different, and further research is needed.

"the articles from this symposium provide evidence that neurological similarities exist in the response of humans (6) and rats (7,9) to foods and to drugs. Two of the reports (6,7), as well as our own work (14–16), suggest that even highly palatable food is not addictive in and of itself. Rather, it is the manner in which the food is presented (i.e., intermittently) and consumed (i.e., repeated, intermittent “gorging”) that appears to entrain the addiction-like process. Such consummatory patterns are associated with increased risk for comorbid complications as well as relapse and make treatment particularly challenging. The topic of food addiction bears study, therefore, to develop fresh approaches to clinical intervention and to advance our understanding of basic mechanisms involved in loss of control."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2714380/

Mod parent down:

>you can't teach empathy

I call bullshit. For example, http://pss.sagepub.com/content/early/2013/05/20/0956797612469537.short and http://www.ncbi.nlm.nih.gov/pubmed/2333803

There are several dozen other studies you can find that show emapthy can be taught in cooperating subjects. Note, especially, that in the second link, it was the affective part of empathy that was increased rather than the cognitive aspect of empathy--the very thing that the doubters presume cannot be influenced (affective part of empathy is usually associated with antisocials/narcissists/etc., whereas cognitive empathy is more affected in autism spectrum disorders and such).

Even in psychopaths, empathy can be increased (as measured directly by imaging of brain activation, rather than relying on self-reporting from unreliable subjects): http://brain.oxfordjournals.org/content/136/8/2550.full?sid=a0dd82b4-a4aa-4af8-a9d2-e3d1ad6d2e97

>Two year olds are sociopaths. Fourteen year olds shouldn't be- they can sometimes be stereotypically *insensitive* due to their brains still developing

More bullshit. The prefrontal cortex doesn't complete development until early 20s and in adults its dysfunction is closely associated with antisocial behavior. There was a study some years ago that showed most children and adolescents, compared to normal adults, have significant impairment in recognizing facial expressions of fear (confusing it with things like surprise or disgust)--just like psychopaths, and that was also linked to incomplete prefrontal cortex development.

Since you're both basically yelling "You're wrong!" at each other and neither one of you has been blessed with an abundance of facts on this topic, I shall dispense some now;

First, let's start with the definition. Sociopathy is a constellation of behaviors, not any one behavior, and you need to exhibit varying degrees of the majority of them for this to be true. Amongst others, these behaviors are: "failing to conform to society's rules, deceitfulness, impulsiveness, reckless endangerment of self or others, and a lack of remorse." The diagnosis is not made before the age of 15. Source: DSM-IV.

While there is a genetic component, it has been demonstrated that abused and neglected children exhibit significantly higher levels of antisocial personality disorder (APD, known to laymen as 'sociopaths'). Source. Research suggests that sociopathy is more a case of 'nurture' than 'nature' -- significant disruptions to hormonal balance, depression, and emotional trauma have all been identified in a significant portion of the clinical population -- too much to dismiss as coincidence.

In adolescents in particular, the failures often orbit around poor parenting and lack of school engagement. In other words, while the parents are primarily responsible, these children are very often also let down by a community and/or school simply unwilling to pick up the slack, as it were.

It is no surprise that teenagers are particularily suseptible to the development of sociopathy; it's been shown that sociopathy's neurological 'core' is the prefrontal cortex. We can actually put people who are sociopathic in an MRI and chart structural changes in the brain in areas relating to judgment, impulsiveness, aggressiveness and decision-making. It is thought that seratonin is the primary neurochemical. This is the same neurotransmitter targetted by anti-depressants. This part of the brain is undergoing rapid change in the adolescent brain, and as such presents a narrow window of opportunity to correct behavioral problems such as sociopathy... or to cause them. Regardless, once the person is an adult, these behavior changes solidify and become largely permanent -- APD is usually a lifelong diagnosis.

--
Now armed with some suitable facts;

... but that's absolutely nothing like this.

Actually, it's exactly like this. Teenagers are moody because their brains are being rewired while they're using them. Imagine trying to patch the kernel of a system while it's being used. In a computer, this usually results in the system crashing or "unexpected behavior". Unsurprisingly... teenagers exhibit similar randomness as neural pathways are rewired. This is a well-known process called Synaptic pruning and it happens at two points in a person's life: At birth until age 2, and again during puberty. Pruning is widely thought to represent learning.

The fact that she made comments like that even *after* the girl died (due to their bullying) indicates pure sociopathy.

I'm afraid that diagnosis cannot be made. You're operating under a large number of assumptions: Firstly, that everyone reacts to death the same way. Secondly, that the prior existing relationship between those people is immaterial in this reaction. Thirdly, that guilt, remorse, etc., are even bona-fide emotions and not simply social constructs. All three of those assumptions are false. If Obama were to be shot and killed tomorrow, many people would be celebrating his death. That doesn't make those people sociopaths. It makes them a great many other things with less than wonderful connotations, but sociopathy isn't on that list. These girls didn't like this other girl; It's not exactly out of profile that her death would not be taken hard.

And regarding guilt, remorse, etc., these are in fact socially-constructed. Guilt can only come from a person who identifies an action which violated their own s

People who are prone to the real suicide are much more quiet about it than some drama queens who are shouting "I'm going to kill myself!" several times a day.

That's a dangerous misconception. Often, but not always, a person may show certain symptoms or behaviors before a suicide attempt, including:... "Talking about death or suicide, or even saying that they want to hurt themselves".

Always take suicide attempts and threats seriously. About one-third of people who try to commit suicide will try again within 1 year. About 10% of people who threaten or try to commit suicide will eventually kill themselves.

The person needs mental health care right away. Do not dismiss the person as just trying to get attention.

Difficult conversations,yes. And here is an even more difficult aspect, because there is no profit in it for the mainstream cancer industry: http://www.lef.org/protocols/cancer/brain_tumor_01.htm
"Vitamin D3, the chemical form of vitamin D made in the skin and sold as a nutritional supplement, calcitriol (1,25-dihydroxy vitamin D), the active form of vitamin D, and various chemical analogs and metabolites of vitamin D, have all been shown to inhibit growth and trigger apoptosis in neuroblastoma and glioma cells (Naveilhan P et al 1994, Baudet C et al 1996, Elias J et al 2003, van Ginkel PR et al 2007)."

Iodine is another thing to consider for helping with cure and prevention, and again is very cheap and not patentable so has few advocates in the cancer industry:
http://brain-cancer-survivor.blogspot.com/2011/12/could-iodine-kill-cancer-cells.html

As Upton Sinclair said: "It is difficult to get a man to understand something, when his salary depends upon his not understanding it!"

Upton Sinclair also wrote a book on using fasting to heal cancer, btw, but what profit is their in advising patients to fast compared to advising them to buy $10K bottles of pills every month?
http://www.healingcancernaturally.com/fasting-cure-for-health.html

But once you have cancer, getting rid of it is iffy no matter what you do. The best thing to do is to prevent it, which again is fairly inexpensive, without much profit for the mainstream medical industry:
http://www.drfuhrman.com/library/article24.aspx

The USA even subsidizes creating cancer through its agricultural policies:
http://www.seriouseats.com/2007/11/the-subsidized-food-pyramid.html
"The Physicians Committee for Responsible Medicine has posted an easy-to-understand visual on its site that shows which foods U.S. tax dollars go to support under the nation's farm bill. It's titled "Why Does a Salad Cost More Than a Big Mac?" and depicts two pyramidsâ"subsidized foods and the old recommended food pyramid. It's interesting to note that the two are almost inversely proportional to each other."

I doubt this level of alleged fraud is common, but it does show the risk of conflict of interest in oncology, where the same doctor prescribing the treatments profits from carrying them out:
http://www.dailykos.com/story/2013/08/07/1229570/-Michigan-doctor-arrested-for-purposely-misdiagnosing-cancer
"In the course of the scheme, prosecutors say Dr. Fata falsified and directed others to falsify documents. MHO billed Medicare for approximately $35 million dollars over a two-year period, approximately $25 of which is attributable to Dr. Fata, federal officials said The complaint further alleges that Dr. Fata directed the administration of unnecessary chemotherapy to patients in remission; deliberate misdiagnosis of patients as having cancer to justify unnecessary cancer treatment; administration of chemotherapy to end-of-life patients who will not benefit from the treatment; deliberate misdiagnosis of patients without cancer to justify expensive testing; fabrication of other diagnoses such as anemia and fatigue to justify unnecessary hematology treatments, and distribution of controlled substances to patients without medical necessity or are administered at dangerous levels."

Conflicts of interest apply to research as well:
"Financial conflicts of interest in economic analyses in oncology."
http://www.ncbi.nlm.nih.gov/pubmed/21441858
"Some financial conf

You don't even need a vaccine to stop from being burned to death in the kitchen. (or worse yet, burning one of those innocent children to death) Just don't cook in your home.

And you can avoid catching chicken pox by avoiding all contact with other people, which is about equally practical.

Fortunately, there is an effective vaccine for one of these problems.

You are wrong that there is no evidence to support the notion that vaccination pushes infection off to adulthood. The vaccine was introduced in 1995, and by 2000/2001 we were already seeing serious failures.

So if vaccination were just pushing infection off to adulthood, we should be seeing a big spike in deaths and hospitalization from chicken pox in adults. Except we aren't

In 1986 and 1987, 2 articles appeared in the literature by physicians from Cook County Hospital in Chicago detailing the extent of patient dumping to that facility (1, 2). The authors defined dumping as “the denial of or limitation in the provision of medical services to a patient for economic reasons and the referral of that patient elsewhere” (1). The majority of such transfers to Cook County Hospital involved patients who were minorities and unemployed. The reason given for the transfer by the sending institution was lack of insurance in 87% of the cases. Only 6% of the patients had given written informed consent for their transfer. Medical service patients who were transferred were twice as likely to die as those treated at the transferring hospital, and 24% of the patients were considered to have been transferred in an unstable condition. It was concluded that this practice was done primarily for financial reasons and that it delayed care and jeopardized the patient's health. This practice was not limited to Chicago but occurred in most large cities with public hospitals. In Dallas, such transfers increased from 70 per month in 1982 to more than 200 per month in 1983 (1).

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1305897/

There is no such thing as "safe" radiation, so eliminating all man-made causes is a good thing, even if the levels are lower than background in some areas.

Citation please? I give you mine:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2663584/

In many places where the background radiation is higher but still at "safe" levels it doesn't seem to be killing people faster. In fact in some places they seem to live longer! Yes it could be due to other factors (diet, lifestyle), but it just shows that at those levels the radiation no longer significantly reduces your lifespan.

Certainly people have adverse reactions to vaccines, as with any medication; I had a penicillin allergy when I was very young that meant I couldn't get certain standard shots, including (I think) MMR. Fortunately medicine is improving so the likelihood of preventable medication-caused harm is reducing. Here is an article on what we know and what alarmists assume.

Yep, this really does demonstrate what to expect from socialized medicine....mainstream doctors using bullshit as medicine. Is working memory training effective? A meta-analytic review. http://www.ncbi.nlm.nih.gov/pubmed/22612437

If you think that the "women, minorities, veterans preference" means anything at all in the real world, please give some examples. Good luck.

What, are you kidding? Look at the rules and regulations for awarding grants and contracts. SBIRs are a good place to start. There are quotas in place whose stated purpose is to incentivize the award of government money to businesses owned by women and minorities. Let me emphasize this: such an outcome is the declared aims of these rules. Government grants and contracts are intended to be based on factors other than merit.

And where's the proof that your simulated neuron is close enough to a real neuron? Weather simulations aren't the same as the weather itself, they can help us predict weather but they are not the same thing. The more accurate the simulation the more it can tell you about the thing being simulated.

Single celled creatures are more complicated than most people appreciate. Many have complex skeletons of a sort. Some even build elaborate shells (and they gather enough material before they reproduce so that they have enough for two shells). The shells are not some random creation parent and child have similar shells: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1193677/pdf/407.pdf

They can't talk, they can't speak, they can't see. But neither can some humans. Not saying they're as smart as humans but I think we underestimate them greatly. Once we learn more about how they think then we'll make more progress on how we think.

Ok, I hope the NIH is good enough for you, because it's what determined my own concern.
here

Einstein was a musician for most of his life. That accounts for the increased thickness of the corpus callosum. Not sure about the size argument. Neanderthals had larger brains than we do.

Well studies have been done which seem to correlate. The abstract implies that intelligent people are more likely to "experiment" though. That's not quite the same thing.

I've read a lot about neuroscience discoveries and interesting abnormalities and didn't know the direct correlation between the corpus collosum thickness and intelligence. Ok, so when someone claims something like this article I think - bah... another stupid claim about Einstein. But this time there is some merit to the claim. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754582/ And yes, his other brain differences were know for a while, so this seems to be a new revelation based on new evidence of the correlation and the discovered photos.

It's not just mutilation anymore.

Check back in 3 years.

A fertilized zygote, on the other hand, usually will.

Back in reality, "Around half of all fertilized eggs die and are lost (aborted) spontaneously, usually before the woman knows she is pregnant."

For more details on 'step e', where the fatty aldehyde is converted to the gasoline alkanes, look up the "cer1 enzyme": http://www.ncbi.nlm.nih.gov/pmc/articles/PMC161066/

This enzyme is used by plants to create waxy coating on their leaves.

I find this to be a great example of what can happen when people are looking cross-disciple for solutions!

For some reason, it's not considered an epidemic when a doctor being paid by insurance companies prescribes methamphetamine manufactured by a pharmaceutical corporation under the brand name "Desoxyn"

Yes it is.

NIH: "The original amphetamine epidemic was generated by the pharmaceutical industry and medical profession as a byproduct of routine commercial drug development and competition" http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2377281/

White House: "The Centers for Disease Control and Prevention has classified prescription drug abuse as an epidemic". http://www.whitehouse.gov/ondcp/prescription-drug-abuse

If by evolution you mean the addition of information via useful mutations in the human genome, it is yet to be observed. What *has* been observed instead is functional deterioration of the genome - see http://rt.com/usa/intelligence-stanford-years-fragile-531/ .

(For a more - vigorous - view, see http://evolutionsciencenow.blogspot.com.au/2013/04/are-humans-getting-better-what-is.html )

So crystallisation via cooling is a "spectacular decrease in entropy", capable of disproving the papers referenced earlier. How did you assess this? By seeing regularity in simple repeating crystal structures versus the liquid blob? By this logic, the regularity of molecules in a solid is evidence of the same thing. But no one calls cooling of a liquid to a solid a "spectacular decrease in entropy".

So the similar size of the earth and the moon are a coincidence...

> There are only a handful of trees left of that age. No way an exponential curve would be smooth with that little data.

You must be very familiar with the details. Anyway, the point is not that there is a smooth curve. The point is that there is a curve which stops abruptly at a time which matching the date of the Genesis flood. There are no trees with more rings. But the oldest trees are *still* growing. So there is no reason that there should not be trees with more rings.

If the ages of the oldest trees is another coincidence, it roughly coincides also with the the span of recorded history and the time since the ancestors of the Danes separated from the ancestors of the Turks.

There are other coincidences.

There is NOT a clear scientific consensus at all.

For example:

http://toxsci.oxfordjournals.org/content/114/1/1.full

and:

http://www.ncbi.nlm.nih.gov/pubmed/21438738

The British Medical Research Council is not some Koch funded faux science organization. This group has supported or hosted over 50 Nobel Laureates in science and medicine including names like Fleming and Crick and Watson.

There is NO mechanism that accounts for the reports of these affects at the extremely low levels reported, and as the above article notes, efforts to reproduce these studies by national labs (not industry supported labs) are very often unsuccessful.

There a lot of serious problems with doing risk assessment for endocrine disruptors.

The first is that there is no known mechanism for most of the effects reported in the literature. Without this mechanism a real science based approach is impossible.

The second issue (and a general problem for that matter) is that many of the studies reported turn out not to be reproducible.

The following articles give some insight into this, relative to BPA which has been (possibly without justification a cause celebre):

http://munews.missouri.edu/news-releases/2013/0102-previous-studies-on-toxic-effects-of-bpa-couldn%E2%80%99t-be-reproduced-says-mu-research-team/

http://www.ncbi.nlm.nih.gov/pubmed/21438738

Only problem with copper is oxidation, requiring maintenance, which is possibly why they switched.

There was a lot of talk about copper recently when a study was published about the possibilities of using copper alloys in hospitals to prevent hospital acquired infections. They noted that over a two year period the copper surfaces didn't seem to tarnish enough to diminish the antimicrobial activity despite the regular cleaning and other contact, so it probably lasts a fair bit longer than two years. That doesn't seem like an unsustainably short period to cycle it over, especially if the surfaces are designed so that the copper can be snapped off and replaced without having to replace the entire bed or whatever the item is.

Here is an overview of the core differences between the human and chimpanzee genomes. The human chromosomes are lined up across the horizontal axis, and the chimp chromosomes are lined up along the vertical axis. Upward diagonal lines indicate the same content, downward diagonal lines are inversion events, where chunks of DNA were flipped as the two species diverged from their common ancestor some six million years ago. When correcting for these inversions, 98.8% of all nucleotides are identical between humans and chimps, accounting for about 37 million changed bases, most of which are at the level of a single nucleotide.

Unfortunately we don't have enough sequenced pre-human genomes to construct a meticulous history at the level you're requesting. I can't say "base a on chromosome b flipped on Tuesday, March 32nd three hundred thousand years ago" because the only other genome we've fully sequenced so far is the Neanderthal one, which has about 99.7% identity or 9 million differences from the average modern-day human, and is only 38,000 years old; all we can do is make diff patches with the genomes we have. If you'd like to compare specific genes to see the differences between human and chimp genes for yourself, you can copy the accession numbers from here into the text box at the top of this form to see the chimp genes that most closely match a given human gene. Try NM_001282628.1 for an example; it only has three single-nucleotide differences in it. The gene it encodes, arylsulfatase E, is vital to bone development, and is well-conserved in all vertebrates, so it makes sense that the differences between the human and chimp copies are minor.

In fact, there's a good chance that they're silent mutations—a substantial fraction of nucleotide changes either don't affect the protein sequence at all (because of redundancies in the translation table) or make unimportant changes, like swapping two very similar amino acids (also because of redundancies.) The existence of a large number of silent mutations between two species is one of the most powerful arguments for a common origin—if life was created from scratch just recently, why the hell are there so many replication mistakes? The number of differences—on the order of millions of errors—requires hundreds of thousands of generations to produce.

For a more dramatic effect, try switching to the full database instead of just the chimpanzee. Looking down the list of hits for NM_001282628.1, you'll see that nearly every vertebrate we know of has a copy of this gene, and the nucleotide sequences are largely identical, but never quite the same. If there are exceptions, then it's most likely because they evolved the capacity to do the same task through a different approach following the loss of the gene.

Here is an overview of the core differences between the human and chimpanzee genomes. The human chromosomes are lined up across the horizontal axis, and the chimp chromosomes are lined up along the vertical axis. Upward diagonal lines indicate the same content, downward diagonal lines are inversion events, where chunks of DNA were flipped as the two species diverged from their common ancestor some six million years ago. When correcting for these inversions, 98.8% of all nucleotides are identical between humans and chimps, accounting for about 37 million changed bases, most of which are at the level of a single nucleotide.

Unfortunately we don't have enough sequenced pre-human genomes to construct a meticulous history at the level you're requesting. I can't say "base a on chromosome b flipped on Tuesday, March 32nd three hundred thousand years ago" because the only other genome we've fully sequenced so far is the Neanderthal one, which has about 99.7% identity or 9 million differences from the average modern-day human, and is only 38,000 years old; all we can do is make diff patches with the genomes we have. If you'd like to compare specific genes to see the differences between human and chimp genes for yourself, you can copy the accession numbers from here into the text box at the top of this form to see the chimp genes that most closely match a given human gene. Try NM_001282628.1 for an example; it only has three single-nucleotide differences in it. The gene it encodes, arylsulfatase E, is vital to bone development, and is well-conserved in all vertebrates, so it makes sense that the differences between the human and chimp copies are minor.

In fact, there's a good chance that they're silent mutations—a substantial fraction of nucleotide changes either don't affect the protein sequence at all (because of redundancies in the translation table) or make unimportant changes, like swapping two very similar amino acids (also because of redundancies.) The existence of a large number of silent mutations between two species is one of the most powerful arguments for a common origin—if life was created from scratch just recently, why the hell are there so many replication mistakes? The number of differences—on the order of millions of errors—requires hundreds of thousands of generations to produce.

For a more dramatic effect, try switching to the full database instead of just the chimpanzee. Looking down the list of hits for NM_001282628.1, you'll see that nearly every vertebrate we know of has a copy of this gene, and the nucleotide sequences are largely identical, but never quite the same. If there are exceptions, then it's most likely because they evolved the capacity to do the same task through a different approach following the loss of the gene.

Here is an overview of the core differences between the human and chimpanzee genomes. The human chromosomes are lined up across the horizontal axis, and the chimp chromosomes are lined up along the vertical axis. Upward diagonal lines indicate the same content, downward diagonal lines are inversion events, where chunks of DNA were flipped as the two species diverged from their common ancestor some six million years ago. When correcting for these inversions, 98.8% of all nucleotides are identical between humans and chimps, accounting for about 37 million changed bases, most of which are at the level of a single nucleotide.

Unfortunately we don't have enough sequenced pre-human genomes to construct a meticulous history at the level you're requesting. I can't say "base a on chromosome b flipped on Tuesday, March 32nd three hundred thousand years ago" because the only other genome we've fully sequenced so far is the Neanderthal one, which has about 99.7% identity or 9 million differences from the average modern-day human, and is only 38,000 years old; all we can do is make diff patches with the genomes we have. If you'd like to compare specific genes to see the differences between human and chimp genes for yourself, you can copy the accession numbers from here into the text box at the top of this form to see the chimp genes that most closely match a given human gene. Try NM_001282628.1 for an example; it only has three single-nucleotide differences in it. The gene it encodes, arylsulfatase E, is vital to bone development, and is well-conserved in all vertebrates, so it makes sense that the differences between the human and chimp copies are minor.

In fact, there's a good chance that they're silent mutations—a substantial fraction of nucleotide changes either don't affect the protein sequence at all (because of redundancies in the translation table) or make unimportant changes, like swapping two very similar amino acids (also because of redundancies.) The existence of a large number of silent mutations between two species is one of the most powerful arguments for a common origin—if life was created from scratch just recently, why the hell are there so many replication mistakes? The number of differences—on the order of millions of errors—requires hundreds of thousands of generations to produce.

For a more dramatic effect, try switching to the full database instead of just the chimpanzee. Looking down the list of hits for NM_001282628.1, you'll see that nearly every vertebrate we know of has a copy of this gene, and the nucleotide sequences are largely identical, but never quite the same. If there are exceptions, then it's most likely because they evolved the capacity to do the same task through a different approach following the loss of the gene.

Here is an overview of the core differences between the human and chimpanzee genomes. The human chromosomes are lined up across the horizontal axis, and the chimp chromosomes are lined up along the vertical axis. Upward diagonal lines indicate the same content, downward diagonal lines are inversion events, where chunks of DNA were flipped as the two species diverged from their common ancestor some six million years ago. When correcting for these inversions, 98.8% of all nucleotides are identical between humans and chimps, accounting for about 37 million changed bases, most of which are at the level of a single nucleotide.

Unfortunately we don't have enough sequenced pre-human genomes to construct a meticulous history at the level you're requesting. I can't say "base a on chromosome b flipped on Tuesday, March 32nd three hundred thousand years ago" because the only other genome we've fully sequenced so far is the Neanderthal one, which has about 99.7% identity or 9 million differences from the average modern-day human, and is only 38,000 years old; all we can do is make diff patches with the genomes we have. If you'd like to compare specific genes to see the differences between human and chimp genes for yourself, you can copy the accession numbers from here into the text box at the top of this form to see the chimp genes that most closely match a given human gene. Try NM_001282628.1 for an example; it only has three single-nucleotide differences in it. The gene it encodes, arylsulfatase E, is vital to bone development, and is well-conserved in all vertebrates, so it makes sense that the differences between the human and chimp copies are minor.

In fact, there's a good chance that they're silent mutations—a substantial fraction of nucleotide changes either don't affect the protein sequence at all (because of redundancies in the translation table) or make unimportant changes, like swapping two very similar amino acids (also because of redundancies.) The existence of a large number of silent mutations between two species is one of the most powerful arguments for a common origin—if life was created from scratch just recently, why the hell are there so many replication mistakes? The number of differences—on the order of millions of errors—requires hundreds of thousands of generations to produce.

For a more dramatic effect, try switching to the full database instead of just the chimpanzee. Looking down the list of hits for NM_001282628.1, you'll see that nearly every vertebrate we know of has a copy of this gene, and the nucleotide sequences are largely identical, but never quite the same. If there are exceptions, then it's most likely because they evolved the capacity to do the same task through a different approach following the loss of the gene.

I'd like to see versions of this with array-of-Kerr-cells in place of the liquid crystal device (for more rapid modulation, at the cost of high voltage drivers), or digital light processors for the mirrors (though the latter are more on/off than continuously adjustable so they might be more limited on what beams they can form).

your wish is my command:
http://www.ncbi.nlm.nih.gov/pubmed/18319825

http://www.ncbi.nlm.nih.gov/pubmed/18319825

Which is why the criminals responsible for this whole charade renamed it 'climate change'.

Wow! I guess they must have had a lot of foresight then to publish this paper in October of 1970:

"Carbon Dioxide and its Role in Climate Change" by George Benton.

Maybe they don't get cancer because they die of heart disease first: Tooth decay can cause heart problems

http://www.abs-cbnnews.com/lifestyle/11/25/10/tooth-decay-can-cause-heart-problems

MANILA, Philippines - Far as your pearly whites may be from your heart, dental experts say a small dental problem can go a long way. In fact, keeping your teeth healthy may just save your life.

-=-=

You know what else protects against cancer? Alzeimer's disease. People who get cancer rarely get Alzeimer's, and people who get Alzeimer's rarely if ever get cancer. see: http://www.nlm.nih.gov/medlineplus/news/fullstory_138596.html

The soil replacement substrate they are testing (arcillite) is highly absorbent and probably is pretreated with the fertilizers. I know that similar experiments (SVET, russian ) were done on the Russion Mir station (my father was leading the team that developed the soil substrate). They used naturally occurring mineral (zeolite) which is extremely good absorbent. You can pretreat it with a fertilizer mix and it will leach small amounts of nutrients and support plant growth for years. All you need to do is add water. The zeolite is also very light - the dry stones will actually float when placed in water, until they absorb enough of it to sink. The zeolites and I assume the arcillite substrate that NASA is testing can also serve as base for soil formation. On long missions you can mix them with waste and let it rot. Because of their absorbent properties the zeolites will actually reduce the smell that comes out of the mix. I would guess that in a confined box with no external supply of fresh air, this would be quite an advantage.

Here are some references for the substrate description and the experiment results.

Everyone's ignoring the fact that vitamin A, like D, are fat-soluble, not water soluble, and so if a large portion of the food intake was this vitamin A rice, there are medical consequences of too *much* of the vitamin.

http://www.niams.nih.gov/Health_Info/Bone/Bone_Health/Nutrition/vitamin_a.asp

            mark

Yes. For starters: http://www.ncbi.nlm.nih.gov/pubmed/11166759

There is reasonable evidence to conclude that they are not harmful http://www.ncbi.nlm.nih.gov/pubmed/23033998

and yet this research concludes the opposite http://www.ncbi.nlm.nih.gov/pubmed/23033998 Governments are so dependent on tax from tobacco and funding from big pharma and big tobacco you have to question their motivations in proposing bans

http://www.ncbi.nlm.nih.gov/pubmed/23033998

I don't know what those guys are doing to the tobacco in manufactured smokes, but it's something evil.

Current research (done by someone I was in biomedical science classes with) suggests that monoamine oxidase inhibitors may have a role in the increased addiction of cigarettes over plain tobacco -- although that article in particular suggests people using roll-your-own tobacco may have a harder time quitting.