The world's first vaccine designed to prevent cancer was not developed by a pharmaceutical company. Instead, its development was funded by public institutions on two continents, including three universities, and the U.S. National Cancer Institute. The vaccine prevents human papillomavirus (HPV), an ailment that can lead to deadly cervical cancer. HPV is spread through sexual contact, and 80% of males and females become infected during their lifetimes. But, thanks the to HPV vaccine, it doesn't have to be that way anymore.

How the HPV vaccine works

The HPV vaccine relies on virus-like particles (VLPs). The VLPs in the HPV vaccine share the same outer protein coat (L1) as human papillomavirus, however, the VLPs do lack the genetic material in HPV necessary to infect a human. The outer protein coat is the key to how the vaccine works. Thanks to the protein coat, the VLPs can assemble in the same way as HPV, and this structural similarity allows the components of the vaccine to produce an immune response without subjecting the patient to the virus in any way. It's not a neutered or dead form of the virus as in the influenza vaccine - it's no virus at all.

3 schools, 4 research groups, & (at least) 4 patents

The creation of the HPV vaccine was an effort two decades in the making. Researchers at Georgetown University are credited with the dominant patent for the the HPV vaccine due to their initial background research, however, the Georgetown team never worked with the virus-like particles. The Georgetown University group showed that the native conformation (the normal form) of L1 protein coat was needed to allow virus-like particles to form.

The U.S. Patent Office also recognizes patent claims from the U.S. National Cancer Institute, the University of Queensland, and the University of Rochester. Researchers at the University of Queensland published data with two different types of protein coats, L1 and L2, and noted that these coats allowed the assembly of virus like particles, but these virus like particles were small and not correctly assembled. This finding pre-dated the Georgetown University publication, and has spurred some controversy concerning the dominant patent.

Researchers at the National Cancer Institute, a branch of the NIH separate and apart from universities, were the first to produce an active virus-like particle that produced an immune response in animals. The NCI researchers also determined that other researchers had been using a mutant of the major HPV L1 capsid, causing slight changes in the manner in which the VLPs formed, thus refining the process.

The University of Rochester team was responsible for the first studies showing an immune response in humans. The University of Queensland research was pioneered by Dr. Ian Frazer in Australia, and sold partial patents to Merck and an Australian company CSL Limited to finance their research and clinical trials. The teams at Georgetown University and the University of Rochester were funded through grants from the National Cancer Institute.

These four groups may not have worked jointly, however, their work (and possible academic rivalry) combined with public funding allowed for quick and efficient discovery and optimization of the VLPs, as most of the major research findings paving the way for the HPV vaccine occurred between 1991 and 1993.

Two versions of the vaccine

Gardisil, the first HPV vaccine on the market, is manufactured by Merck and protects against four different strains of HPV. This protection covers HPV-16 and HPV-18, with these causing 70% of cervical cancer cases, cases which kill as many as 300,000 women annually. HPV-16 has also been linked to oropharyngeal cancer. Gardisil also protects against HPV-6 and HPV-11, guarding against 90% of genital warts. Protection against general warts and a recent FDA statement showing Gardisil to prevent anal and oropharyngeal cancer has increased demand amongst both males and females.

Cervarix, produced by GlaxosmithKline and approved for use in the United States in 2009 after several years of use in other areas of the world, protects only against HPV-16 and HPV-18, and thus lacks protection against genital warts. Despite this lack of protection against the physical attributes of sexually transmitted disease, one recent National Cancer Institute study showed that two of the mandated three shots of Cervarix may be sufficient for protection. This is quite the finding, as the third dose is taken six months after the initial injection, and likely to be skipped by the patient. Additionally, Cevarix has been shown to be effective over 7 years after administration.

Arguing against the HPV Vaccine

The suggestion that boys and young men receive the HPV vaccine has been met with controversy. Dr. William Schaffner, chairman of the Department of Preventive Medicine at Vanderbilt University School of Medicine, recently stated his support for administering the vaccine to boys and young men, emphasizing how far basic research has come:

This is cancer, for Pete's sake […] A vaccine against cancer was the dream of our youth.

You might not like shots, but it's hard to argue against getting the HPV vaccine. There is no dead or neutered virus involved - there is no genetic material in the vaccine at all. The HPV vaccine a great example of public funding and several universities putting the parts together quickly and saving many lives in the process.

Images courtesy of the World Health Organization, Medscape, and GlaxoSmithKline. Sources linked within article.

The world's first vaccine designed to prevent cancer was not developed by a pharmaceutical company. Instead, its development was funded by public institutions on two continents, including three universities, and the U.S. National Cancer Institute. The vaccine prevents human papillomavirus (HPV), an ailment that can lead to deadly cervical cancer. HPV is spread through sexual contact, and 80% of males and females become infected during their lifetimes. But, thanks the to HPV vaccine, it doesn't have to be that way anymore.

How the HPV vaccine works

The HPV vaccine relies on virus-like particles (VLPs). The VLPs in the HPV vaccine share the same outer protein coat (L1) as human papillomavirus, however, the VLPs do lack the genetic material in HPV necessary to infect a human. The outer protein coat is the key to how the vaccine works. Thanks to the protein coat, the VLPs can assemble in the same way as HPV, and this structural similarity allows the components of the vaccine to produce an immune response without subjecting the patient to the virus in any way. It's not a neutered or dead form of the virus as in the influenza vaccine - it's no virus at all.

3 schools, 4 research groups, & (at least) 4 patents

The creation of the HPV vaccine was an effort two decades in the making. Researchers at Georgetown University are credited with the dominant patent for the the HPV vaccine due to their initial background research, however, the Georgetown team never worked with the virus-like particles. The Georgetown University group showed that the native conformation (the normal form) of L1 protein coat was needed to allow virus-like particles to form.

The U.S. Patent Office also recognizes patent claims from the U.S. National Cancer Institute, the University of Queensland, and the University of Rochester. Researchers at the University of Queensland published data with two different types of protein coats, L1 and L2, and noted that these coats allowed the assembly of virus like particles, but these virus like particles were small and not correctly assembled. This finding pre-dated the Georgetown University publication, and has spurred some controversy concerning the dominant patent.

Researchers at the National Cancer Institute, a branch of the NIH separate and apart from universities, were the first to produce an active virus-like particle that produced an immune response in animals. The NCI researchers also determined that other researchers had been using a mutant of the major HPV L1 capsid, causing slight changes in the manner in which the VLPs formed, thus refining the process.

The University of Rochester team was responsible for the first studies showing an immune response in humans. The University of Queensland research was pioneered by Dr. Ian Frazer in Australia, and sold partial patents to Merck and an Australian company CSL Limited to finance their research and clinical trials. The teams at Georgetown University and the University of Rochester were funded through grants from the National Cancer Institute.

These four groups may not have worked jointly, however, their work (and possible academic rivalry) combined with public funding allowed for quick and efficient discovery and optimization of the VLPs, as most of the major research findings paving the way for the HPV vaccine occurred between 1991 and 1993.

Two versions of the vaccine

Gardisil, the first HPV vaccine on the market, is manufactured by Merck and protects against four different strains of HPV. This protection covers HPV-16 and HPV-18, with these causing 70% of cervical cancer cases, cases which kill as many as 300,000 women annually. HPV-16 has also been linked to oropharyngeal cancer. Gardisil also protects against HPV-6 and HPV-11, guarding against 90% of genital warts. Protection against general warts and a recent FDA statement showing Gardisil to prevent anal and oropharyngeal cancer has increased demand amongst both males and females.

Cervarix, produced by GlaxosmithKline and approved for use in the United States in 2009 after several years of use in other areas of the world, protects only against HPV-16 and HPV-18, and thus lacks protection against genital warts. Despite this lack of protection against the physical attributes of sexually transmitted disease, one recent National Cancer Institute study showed that two of the mandated three shots of Cervarix may be sufficient for protection. This is quite the finding, as the third dose is taken six months after the initial injection, and likely to be skipped by the patient. Additionally, Cevarix has been shown to be effective over 7 years after administration.

Arguing against the HPV Vaccine

The suggestion that boys and young men receive the HPV vaccine has been met with controversy. Dr. William Schaffner, chairman of the Department of Preventive Medicine at Vanderbilt University School of Medicine, recently stated his support for administering the vaccine to boys and young men, emphasizing how far basic research has come:

This is cancer, for Pete's sake […] A vaccine against cancer was the dream of our youth.

You might not like shots, but it's hard to argue against getting the HPV vaccine. There is no dead or neutered virus involved - there is no genetic material in the vaccine at all. The HPV vaccine a great example of public funding and several universities putting the parts together quickly and saving many lives in the process.

Images courtesy of the World Health Organization, Medscape, and GlaxoSmithKline. Sources linked within article.

After 1978, two strangely related things happened: a new set of regulations for processed meat limited the amount of nitrite used in hot dogs, forcing manufacturers to add ascorbate or erythorbate instead. And the following that year, there was a major dropoff in colon cancer deaths. Now, researchers are questioning the link between the two.

Nitrite preserved processed meats are loaded with nonvolatile N-nitroso compounds, but the addition of ascorbate and erythorbate replaced them, with only 1/90th of the amount remaining afterwards. There has been a significant amount of work on the link to processed meat with colorectal cancer, especially with the presence of nitrates and nitrites. The thing is that if this correlation was iron clad, then the there would have been a huge drop in the incidence of the cancer with the government regulation. Instead, there's been a major drop in the deaths from the disease — which is something very different. So while fewer people are dying of colon cancer, the drop in nitrites doesn't seem to have meant fewer people getting it.

"The drop in N-nitroso compound content caused by the mandated changes in processed meat should have been accompanied by a drop in the incidence of colon cancer," said Professor Sidney S. Mirvish, and the reduction in deaths "may have been due mostly to earlier detection and better treatment of this disease."

UPDATE: An earlier version of this article significantly misinterpreted part of the study — which was my mistake. It has been updated and corrected. Apologies.

Photo by Kenneth Sponsler via Shutterstock

After 1978, two strangely related things happened: a new set of regulations for processed meat limited the amount of nitrite used in hot dogs, forcing manufacturers to add ascorbate or erythorbate instead. And the following that year, there was a major dropoff in colon cancer deaths. Now, researchers are questioning the link between the two.

Nitrite preserved processed meats are loaded with nonvolatile N-nitroso compounds, but the addition of ascorbate and erythorbate replaced them, with only 1/90th of the amount remaining afterwards. There has been a significant amount of work on the link to processed meat with colorectal cancer, especially with the presence of nitrates and nitrites. The thing is that if this correlation was iron clad, then the there would have been a huge drop in the incidence of the cancer with the government regulation. Instead, there's been a major drop in the deaths from the disease — which is something very different. So while fewer people are dying of colon cancer, the drop in nitrites doesn't seem to have meant fewer people getting it.

"The drop in N-nitroso compound content caused by the mandated changes in processed meat should have been accompanied by a drop in the incidence of colon cancer," said Professor Sidney S. Mirvish, and the reduction in deaths "may have been due mostly to earlier detection and better treatment of this disease."

UPDATE: An earlier version of this article significantly misinterpreted part of the study — which was my mistake. It has been updated and corrected. Apologies.

Photo by Kenneth Sponsler via Shutterstock

Even in decidedly "wealthy" countries, human health is not always guaranteed. In fact, studies show that the best indicator of a country's health is not its overall wealth, but how that wealth is distributed. Time Magazine's Maia Szalavitz reports:

Imagine there was one changeable factor that affected virtually every measure of a country's health- including life expectancy, crime rates, addiction, obesity, infant mortality, stroke, academic achievement, happiness and even overall prosperity. Indeed, this factor actually exists.

It's called economic inequality. A growing body of research suggests that such inequality - more so than income or absolute wealth alone — has a profound influence on a population's health, in every socioeconomic group from rich to middle class to poor.

Economic inequality is measured by looking at the distribution of wealth and income in a society, not the general wealth of a country. At a basic level, a country's overall economic success does predict its people's well-being, but the healthiest and happiest countries in the world are not the richest. Rather, they are countries where wealth is shared widely and more equally.

One of the most obvious ways that economic equality may improve a country's overall health is by improving access to health care for all of its citizens, but Szalavitz writes that poor overall health manages to persist, "even in countries with national health services." So from where, exactly, does the negative correlation between economic inequality and public health stem?

"The roots of the problem," write Szalavitz,"appear to reach deeper than [access to public health care]. Indeed, they may go back to the dominance hierarchies of our primate ancestors."

Read the rest of Szalavitz's excellent piece over at TIME.
Top image via

Despite numerous studies indicating that cell phones pose no health risk to their users, a few studies have been released that suggest prolonged use might contribute to brain cancer. For the World Health Organization, that was enough to declare the phones "possibly carcinogenic" and to call for further studies on the link.

At least one of these studies was already in the works. Some specific features of how Denmark tracks its citizens have made that nation a convenient laboratory for long-term population studies. Now, one study has looked at almost the entire Danish adult population and found that having a cell phone doesn't seem to be associated with any additional risk of brain cancers.

Read the comments on this post

Earlier today, the 2011 Nobel Prize in Physiology or Medicine was awarded to Bruce A. Beutler and Jules A. Hoffmann (pictured left and center, respectively) "for their discoveries concerning the activation of innate immunity;" and to Ralph M. Steinman "for his discovery of the dendritic cell and its role in adaptive immunity."

Steinman, who passed away on Friday after an extended bout with pancreatic cancer, becomes the first person to ever be awarded a Nobel Prize in Physiology or Medicine posthumously.

It bears mentioning that Steinman — who, like Beutler & Hoffman, was recognized for his contributions to the field of immunology — was actually diagnosed with pancreatic cancer years ago, but extended his life by using a dendritic-cell based immunotherapy (you know, that thing he was considered Nobel-worthy for in the first place) of his own design.

The announcement was first issued early this morning by the Nobel Foundation, which was, at the time, unaware of Steinman's recent passing. Since 1974, the statutes of the Nobel Foundation have indicated that "work produced by a person since deceased shall not be considered for an award. If, however, a prizewinner dies before he has received the prize, then the prize may be presented."

The thing is, the Nobel Assembly decided to honor Steinman with a Nobel Prize after he passed away; they just weren't aware of it at the time. This put the Assembly in a situation that they have since described as "unprecedented in the history of the Nobel Prize." Discussions over whether or not to award the prize to Steinman posthumously were held just a few hours ago.

Fortunately, the Assembly had the good sense to stick with this morning's announcement, and have since issued a statement confirming that their initial decision will remain unchanged.

Top images via Nobelprize.org

Read more of this story at Slashdot.

We blame sugar for adding extra calories to almost anything we purchase in the grocery store, and call sugary snacks "junk food." But is sugar really junk? Let's take a look at some common myths about sugar, and find out why there are good reasons for you to keep natural sugars as a part of your diet.

Myth: All sugars are the same.

Fact: Different sugars have different properties and degrees of sweetness.

Sugar comes in many forms. Common table sugar is sucrose, a disaccharide of glucose and fructose, each of which have different properties. Fructose is often called a "fruit sugar" as it is found in honey, berries, and vegetables. Glucose and galactose also accompany fructose as a naturally occurring sugar, however, these naturally occurring sugars are often forsaken for artificial sweeteners, which lack the caloric and other bodily advantages of naturally occurring sugars.

Fructose is considerably sweeter than other naturally-occurring sugars, with fructose being over 1.5 times as sweet as sucrose, over twice as sweet as glucose, and six times sweeter than galactose. Fructose also has a reasonably low manufacturing cost, leading it to be one of the main natural sweeteners used in manufacturing processes.

Myth: Sugar is bad and not a useful part of your diet.

Fact: You need glucose.

Glucose is used as an energy source by almost every organism. Glucose is used by your body's cells as a very efficient energy source. For example, via the the Krebs Cycle, a single molecule of glucose yields a net gain of two molecules of ATP through anaerobic respiration, and 34 molecules of ATP through aerobic respiration.

Glucose is also a valuable precursor for several types of biological molecules; including lipids, amino acids, and cellulose, providing a valuable building block that can be readily used by almost any molecule. The synthesis of glucose was not able to be reproduced in vitro until the late 1800s, with Emil Fischer winning the 1902 Nobel Prize in Chemistry for his contributions to the synthesis of glucose and other naturally occurring sugars.

Myth: Sugar has little impact on humans other than acting as a sweetener.

Fact: Your brain runs on sugar.

You brain's main supply of energy is the monosaccharide glucose. While your brain only weighs between 3 to 5 pounds, it makes use of approximately 15-20% of your body's daily caloric needs. It has been long thought that the glucose was consumed as a function of cognitive experience, and research on rats shows that when a more cognitively challenging task is placed before them, more glucose is depleted. This phenomenon also appears to extend to humans.

In the journal article Glucose, memory, and aging, published by the American Journal of Clinical Nutrition, researchers observed that elderly patients who were given lemonade sweetened with glucose experienced a nearly two fold increase in short term memory when asked to recall a prose passage compared to those who drank lemonade sweetened with the artificial sweetener saccharin (also known by the brand name of "Sweet'N Low"). Additionally, saccharin has no calories.

Glucose has also been shown to have a large impact on self-control and behavior, with limited supplies causing a quick falloff in behavioral stability at times. I like to call this phenomenon "hanger", hungry-anger, when observed in friends and loved ones.

In Sum, Sugar is your Friend

So, sugar isn't all that bad, and honestly, if you want to perform a series of cognitively difficult tasks, you'll be depleting your resources quickly. Individuals with pre-existing conditions like diabetes need to watch their sugar intake, but for the individuals without such ailments, sugar is your friend, not your enemy.

Top photo by Liv friis-larsen via Shutterstock.

Scientists have known for some time that dogfish sharks, like the one pictured up top, naturally produce a broad-spectrum antibiotic called squalamine in their livers. Now, new research into the cellular function of squalamine reveals how it also confers a broad-spectrum antiviral benefit for the shark — one we humans could benefit from, as well.

Many sharks demonstrate a natural immunity to numerous forms of viral infection, even in the absence of a rapidly adapting immune system like ours. This observation got University of Pennsylvania geneticist Michael Zasloff thinking: what if researchers could identify the molecule (or molecules) responsible for conferring this antiviral characteristic?

"I was interested in sharks because of their seemingly primitive but effective immune system." Explains Zasloff. "No-one could explain why the shark was so hardy."

The research team figured that a good place to start looking would be the protein squalamine. Since its discovery in the livers of dogfish sharks 1993, squalamine has received quite a bit of attention for its antibacterial and antitumorigenic properties.

Some of the most recent research surrounding squalamine has revealed that it is also capable of displacing proteins commonly found anchored in cell membranes. (A cell's membrane is the barrier separating its insides from the outside environment, including other cells.) Zasloff hypothesized that squalamine's ability to displace membrane-anchored proteins could grant it antiviral properties, as well.

Zasloff and his colleagues explain their reasoning in the latest issue of Proceedings of the National Academy of Sciences:

Many viruses enter cells through engagement of [membrane-anchored proteins]...Displacement of key proteins anchored through electrostatic forces (of host or viral origin) from the cytoplasmic face of the plasma membrane might interfere with [viral] entry, protein synthesis, virion assembly, virion budding , or other steps in the viral replication cycle.

In other words, the researchers hypothesized that squalamine could interfere with a virus's ability to not only enter and infect healthy cells, but to replicate and propagate, as well.

And the researchers' results suggest that squalamine does exactly that. In tissue cultures and animal models, squalamine was shown to control — and, in some cases, cure — infections by hepatitis B, hepatitus D, yellow fever, dengue virus, Eastern equine encephalitus virus, and murine cytomegalovirus.

Zasloff's team says it has yet to optimize squalamine dosing in any of the animal models, and therefore does not know the maximum therapeutic benefit that can be achieved using squalamine, but their initial results are very encouraging.

The researchers also note that squalamine has already been studied in several phase II clinical trials, and has a known safety profile in humans. Given this, the researchers emphasize how important it is that the broad antiviral properties of squalamine be investigated further.

"Squalamine appears to protect against viruses that attack the liver and blood tissues, and other similar compounds that we know exist in the shark likely protect against respiratory viral infections," explains Zasloff. He continues:

We may be able to harness the shark's novel immune system to turn all of these antiviral compounds into agents that protect humans against a wide variety of viruses. That would be revolutionary.

While many antibacterial agents exist, doctors have few antiviral drugs to help their patients, and few of those are broadly active.

Proceedings of the National Academy of Sciences via BBC
Top image via

From the British Medical Journal, Aug 27, 1949, where Dr. B.B. Rapackl describes a case he encountered in Poland in 1936.

"The patient was admitted to hospital with acute cystitis. Cystoscopy confirmed this diagnosis, and to my great surprise revealed a blue-tinted twisted Christmas candle floating on top of the liquid (‘rivanol') which had been injected into the bladder for the purpose of the examination."

But, readers may be wondering, exactly how did it get there? Here's how:

"When the patient was asked if he himself had introduced the candle into the urethra, he reluctantly admitted that two days previously, while drunk, he had had intercourse with a prostitute whom he could not pay. She in her anger had inserted the candle while he was asleep."

Read full, albeit brief, details in the monograph (it's on page 2 of the .pdf)

This post originally appeared on Improbable Research. Image via.

Cancer vaccines may come sooner than you think. And each vaccine will be tailor-made for a specific kind of cancer. This isn't just a theory anymore. It's been done.

A group of medical researchers in the U.K. and the U.S. have successfully cured prostate cancer in mice using a vaccine made partly from healthy human prostate DNA, delivered inside virus shells. This treatment could come to replace toxic chemotherapies, curing cancer with no painful side-effects.

The researchers injected the mice with virus shells (the outer skin of viruses) packed with "libraries" of DNA made up partly of DNA taken from healthy prostate. The researchers believed that delivering the DNA inside viruses would essentially trick the mouse immune system, sending it into overdrive to produce antibodies tailor-made to attack cancers of the prostate. And their theory turned out to be correct. The mice produced antibodies which attacked their cancerous tumors, effectively eliminating the cancer. Because this vaccine's DNA libraries were tailor-made for prostate cancer, however, it also prevented the mice from producing antigens that attacked other organs in their bodies.

According to the Mayo Clinic, where some of the research took place:

All infections, allergens and tissues, including tumors, have a unique fingerprint called an antigen — a molecular protein tag that triggers a response from the body's immune system. Dr. [Richard] Vile deployed the human vaccine prostate cancer antigens through the mutated VSV vector to raise a full-on assault from the mice's T-cells. After exposure to the mutated viruses, the animals' immune systems recognized the antigens expressed in the virus and produced a potent immune response to attack the prostate tumors.

"Nobody really knows how many antigens the immune system can really see on tumor cells," says Dr. Vile. "By expressing all of these proteins in highly immunogenic viruses, we increased their visibility to the immune system. The immune system now thinks it is being invaded by the viruses, which are expressing cancer-related antigens that should be eliminated."

The big question now is whether this therapy could work in humans. Clinical trials that would lead to using this therapy on humans could begin in two years.

Read the full scientific article via Nature Medicine.

Image via Sebastian Kaulitzki/Shutterstock

When in a cardiac emergency, your body turns your own worst fears against you. The more acutely you feel fear, the worse your heart problem gets. It's like the plot of IT, but without the bad special effects.

One of first books to really scare me was a children's story called Ronia, The Robber's Daughter. It was set in a magical wood, and that wood was populated by various magical creatures. One group of those creatures was called The Gray Dwarves. They would be harmless, and run away from anyone who even shouted at them, as long as that person was not afraid. If they were afraid, the creatures would get vicious, and claw, bite, and pick-axe the person to death. That trope has been picked up in a lot of horror stories. IT involved a creature that would take the form of anyone's worst fears. A Dollhouse episode featured a creature that would come after people in a computer program if they felt too much fear. But of course, that doesn't work in the real world.

Oh, but it does.

Over two years, hospital employees conducted a study that measured the fear of death of a group of people coming into the hospital with a temporarily blocked coronary artery. They also measured the level of each patient's tumour necrosis factor alpha (TNF) molecule. This molecule increases system-wide inflamation, which has been shown to damage the heart. They found that the people who reported high levels of fear had four-fold increase in inflammatory response independent of the actual severity of their condition. This worsened the episode, and not just for the moment. Three weeks later, people with high levels of fear showed low cortisol levels and low heart rate variability. Cortisol is a stress hormone. Low levels of it show that bodily inflammation is still high, making things harder on the heart. Heart rate variability serves as a measure of heart function. When the heart can't adjust well to different circumstances, heart rate variability is low. Both of these factors are bad signs.

The orchestrators of the study at St. George's Hospital in London aren't sure whether the treating the inflammation itself would have effect, or whether they would need to treat the patient's emotional response as well. For the time being they encourage doctors to reassure their patients, and encourage them to talk about their emotional state. They also want people to know that major strides in medicine make coronary artery blockage a treatable phenomenon. Although it should be treated as an emergency, it is not a harbinger of doom.

The lesson I'm taking from this is the same thing I took from the book: Fearing something makes it happen. Be afraid.

Read the full scientific article via European Heart Journal

Timothy Brown was diagnosed with HIV in the ’90s. In 2006, he found that a new, unrelated disease threatened his life: leukemia. After chemo failed, doctors resorted to a bone marrow transplant. That transplant erased any trace of HIV from his body, and may hold the secret of curing AIDS.

If you suffer frequent migraines, you probably already know that tinted lenses are your friend - but now we have scientific proof. Precision tinted lenses have been known for years to provide relief for migraine sufferers and people hit with certain reading difficulties, and now we have the fMRI scans to prove it.

For some people, viewing striped patterns like this one can be enough to trigger a migraine, and for others it can even trigger a seizure due to the illusions of shifting color and motion. When you go in for precision tinted lenses, doctors test your eyes to find the perfect hue and saturation that can counteract this effect, reducing the eye-melting optical illusion to something you can handle, and hopefully reducing your chances of getting an excruciating headache too. It's also thought that some people's dyslexia is caused by a similar problem, so tinted lenses can help them too.

New research has finally put these theories to the test, providing solid evidence that this improvement exists in the real world. The study compared the fMRI scans of migraine sufferers both with and without the colored lenses. When they had the spectacles on, there was reduced cortical activation in the visual area of the occipital cortex of the brain, which is associated with the onset of migraine.

If you have trouble reading because of visual distortion or get horrible migraines from looking at certain patterns, it might be time to swing by your optometrist and get some sweet looking sunglasses.

We all have flourishing bacterial ecosystems in our intestines filled with thousands of microbes. But these gut ecosystems only come in three types. And the type you have may influence the kind of life you lead.

Bacteria are a crucial part of human digestion. Hundreds of billions of them live in our stomachs and intestines, many helping us digest food. With the many different kinds of bacteria, and the many different types and habits of people, it would seem like each stomach and intestines would be unique - a less poetic metaphor for human individuality than a snowflake, but a more apt one. This, however, is not the case. We're far more uniform inside than we are outside. Human gut bacteria ecosystems fall into three different types: Bacteroides, Prevotella and Ruminococcus, each named for the bacteria that rules the roost.

Scientists believe that the reason for this conformity is that our guts can only configure themselves into a limited number of habitats for bacteria. In one habitat, one type of bacteria can dominate - in another, they are forced into a more niche group. Three different gut types is all that humanity can muster.

The ruling bacteria may influence our bodies, too. Gut types have been associated with different physical and medical conditions in people. A recent study found some bacteria process food more efficiently than others - this leaves more calories for their human hosts, and so they may have trouble losing weight. Another study found a correlation between certain bacterial strains and diabetes.

So do our stomachs create us or do we create them? Scientists aren't sure yet. All they've found is correlation - with no word on cause. They also don't know if people could change their gut ecosystems through diet, exercise, or medication.

Read scientific articles on your gut ecosystem in PLOS and Nature.

Illustration by Christian Darkin/Shutterstock

What you're looking at are neurons grown from a schizophrenic person. An incredible study, published today in Nature, reveals how scientists grew schizophrenic brain cells to understand the inner workings of this still-mysterious neurological disorder.

A team of scientists from research institutes across the US collaborated to conduct this first-of-a-kind experiment. Schizophrenia is known to be a genetic disease in the majority of cases, and the researchers drew their samples from the skin of four people with clear signs of genetic schizophrenia. Three were from families where one parent and all their siblings were also schizophrenic, and one had been diagnosed with schizophrenia at the age of 6. The scientists "reprogrammed" these cells to become stem cells, then neurons, creating small colonies of cells whose genetic profile exactly matches schizophrenic neurons.

Over a period of weeks, they watched the cells develop, testing them to see how they differed from a control group of cells. They already knew from previous studies that schizophrenic neurons don't form many connections with other neurons, and indeed this was exactly what they found. Neural connections, which are electrical and chemical links between cells called synapses, allow your brain to form new memories, learn, and come up with new ideas. (You can see them in the fine threads between neurons in the pictures that illustrate this story.) But schizophrenic neurons don't reach out to each other.

And the research team now has a much better picture of why this is. Partly it's because schizophrenic neurons are low on proteins that help build those connections. But the researchers also found unusual behavior in genes needed to regulate two cell processes (called "signalling pathways") that help neurons communicate with each other. What it all boils down to is that schizophrenic neurons suffer from a number of problems, all of which make it harder for them to create the kind of dense neural network your brain needs.

At left, you can see two neural cultures - on the left is the control group and on the right are the schizophrenic cells. Note that the schizophrenic cells have formed far fewer connections than the control group has.

The researchers also tested 5 antipsychotic drugs on the neurons, and found that only loxapine helped the cells form more connections with each other.

In a technical summary, the authors write:

Schizophrenic human-induced pluripotent stem cell neurons showed diminished neuronal connectivity in conjunction with decreased neurite number, PSD95-protein levels and glutamate receptor expression. Gene expression profiles of SCZD hiPSC neurons identified altered expression of many components of the cyclic AMP and WNT signalling pathways. Key cellular and molecular elements of the SCZD phenotype were ameliorated following treatment of SCZD hiPSC neurons with the antipsychotic loxapine.

So what's the upshot? We know that most of the problems in schizophrenic neurons come from an inability to form neural connections, and now we know that these problems are caused by a very complicated set of factors. There is no "schizophrenia gene." And there is no one type of neurological damage that leads to schizophrenia. The good news is that we have a detailed cellular model of one form of schizophrenia now, and what these researchers have found will help others in the field get closer and closer to a therapy that might one day reprogram schizophrenic neurons to be more like typical neurons, forming a web of connections with their fellow cells in the brain.

Read the full scientific paper via Nature

Recently scientists staged a demonstration in which flesh-eating bacteria died off in droves when placed on a copper surface. Find out why copper engages in bactericide.

Hospitals are necessary and efficient institutions meant to gather and train a variety of experts in order to serve any sick person who comes in. They're also festering pits of infection. It's not really their fault. They just have a huge number of very sick people, all of whom are visited by medical staff, administrative personnel, and facilities staff who continue to move through the building, collecting bugs as they go. Though hospitals institute hygienic policies, they remain one of the places where people are at the highest risk for infection. In fact, one of the major places that people pick up MRSA, or flesh-eating bacteria, is in a hospital.

MRSA is notoriously hard to kill, and often requires surgery and stints in hyperbaric chambers. This is why a demonstration of MRSA dying off on a copper was so dramatic. Most instruments in hospitals are stainless steel - a material that does not require much upkeep, is strong, and is easy to shape. The anti-microbial properties of copper make it a tempting alternative. Simple dry copper, and certain copper alloys, kill of bacteria after a few minutes of contact.

Copper's attack on cells is not confined to one approach. It's a renaissance killer, and it unleashes a multifaceted wave of destruction. First, it storms the cell. Cells maintain a certain voltage difference between their bodies and the outside world. The cell wall keeps this difference in electrical potential going. Copper manages to let the electrical energy in the cell flow through to the outside world, short circuiting the cell and weakening the wall. Copper ions also tend to react with oxygen (this causes the green patina that appears on the surface of copper pennies or the Statue of Liberty). If it reacts with oxygen while in contact with certain cell proteins or fatty acids, the whole thing turns into a version of the green patina and the cell wall is 'rusted' away.

Once the cell wall is destroyed, there's free flow into and out of the cell. Potassium and glutamate tend to flow out, draining the cell of needed components. Copper ions flow in. They bind to enzymes in the cell, causing the enzymes to become inactive, and disrupting nutrient processing and cell recreation. The cell is usually dead in minutes.

Various organizations, usually organizations with a lot of copper to sell, are pushing to have things like hand rails, beds, and doorknobs resurfaced with copper or copper alloys, especially in hospitals. Since copper is harmless to humans, it would be a painless way to reduce infections. Although copper tarnishes, it still manages to kill bacteria, and is sometimes shown to kill more bacteria if it looks a little grody. Alternately, doctors, nurses, and staffers could just try to handle a lot of pre-1982 pennies. Those who want to see MRSA die on copper can check out a video of it here.

Via Science Daily, Antimicrobial Copper times two, and Antimicrobial Touch Surface.