Smithsonian.com

The mummy of Esankh, male (1070-712 BCE), undergoes CT scanning (credit: Dr. Michael Miyamoto/UC San Diego)

Heart disease may appear to be a recent problem, brought on by the processed foods and sedentary lifestyles of modern living, but it’s been plaguing humanity since ancient times, according to a new study in the Journal of the American Medical Association.

A team of scientists from the United States and Egypt sent 22 mummies from the Egyptian National Museum of Antiquities in Cairo–some of which were more than 3,000 years old–through a CT scanner. They could see cardiovascular tissue in 16 of the mummies. Five definitely had atherosclerosis (calcification in the arteries), and four more probably had it. Heart disease was more common among the mummies of older individuals than those who died before they reached the age of 45. Some mummies had calcification in multiple arteries.

Risk factors for heart disease include tobacco smoking and eating processed foods, but these couldn’t have contributed to the mummies’ atherosclerosis as tobacco and processed foods weren’t found in Egypt at that time. A sedentary lifestyle is another risk factor, but the study’s authors say that even though the mummies were Egyptians of high social status, they were unlikely to have been sedentary. But a further risk factor is diet, and Egyptians of high social status would have eaten meat, including beef, duck and goose.

I guess this is something to consider on my next trip to the burger joint.

weed chainsaw massacre (courtesy of flickr user 19melissa68)

Here’s a shocker: Horror films like Texas Chainsaw Massacre don’t get the chainsaw spatter right, according to the Journal of Forensic Sciences.

The reason for the study is sad—a woman was reported missing in 2005, and the police found evidence that she had been killed and dismembered in her basement (a few dabs of fresh paint on the walls, small pieces of bone, a receipt for an electric chainsaw). The investigators, possibly having watched a few too many horror films, didn’t think that there was enough blood and tissue spatter in the small room if a human body had been dismembered there by someone wielding a small chainsaw. And there was the question of whether or not the chainsaw itself was powerful enough to accomplish the job without getting stuck in flesh and bone.

A University of South Dakota pathologist got involved. He obtained the same kind of chainsaw indicated in the receipt and a 200-pound female pig, deceased, and created a room the approximate size of the basement using white sheets. He let the pig rest for two days to simulate the time between when the woman had been reported missing and when the chainsaw was purchased. And then he started hacking away.

The chainsaw was certainly powerful enough to cut through the tissue and bone. And the pathologist discovered that if the blade was held parallel to the floor there was very little spatter, similar to what was found at the crime scene. (Vertical positioning of the blade or use of a freshly killed pig increased the amount of spatter on the sheets.) The researcher concluded:

These experiments have shown that a human body may be easily dismembered with a chainsaw, even a smaller electric-powered model….Despite popular beliefs fueled by crime scene shows on television and recent Chainsaw Massacre movies, postmortem dismemberment does not necessarily produce a large amount of blood spatter at a dismemberment scene….With a horizontally oriented chainsaw, therefore, the majority of the tissue and blood will be found on the ground beneath the saw. If the chainsaw discharge chute, however, is not directed towards the ground, then a large volume of blood and tissue, and subsequent spatter, could be expected some distance from the saw.

Something to consider when writing or filming your next scary movie.

H1N1 (swine) flu is in the news again (courtesy of flickr user Dr Craig)

Around the country, people are lining up to be vaccinated against the H1N1 flu virus. Surprising Science has spent the last three days discussing the history and science of vaccines (see A Brief History and How Vaccines Work, Success Stories, and A History of Vaccine Backlash). Today we answer some of the more common questions about the swine flu vaccine.

Who should get the H1N1 flu vaccine?

There is currently not enough vaccine for everyone who wants it. Vaccines take time to produce and this one has been rolling off the line for just a few weeks. As of Tuesday there were about 22.4 million doses available around the United States. The goal is to have 250 million doses by the end of flu season next spring. The Centers for Disease Control and Prevention have recommended that certain groups get vaccinated first:
•    pregnant women
•    people who live with or care for children under six months of age
•    young people age six months to 24 years
•    people 25 to 64 who are at higher risk for flu complications due to a health condition or compromised immune system
•    health care and emergency medical service personnel

Why are these groups first?

Pregnant women and young people seem to be especially vulnerable to the H1N1 virus. Babies under six months of age cannot be vaccinated, so it is important to limit their exposure to the virus by vaccinating people who care for them. People with certain health conditions or who have a compromised immune system have a higher risk of having serious flu complications if they get the flu. And medical personnel are the people most likely to come in contact with the virus.

What if I’m not in one of these groups?

Wait your turn. There will be enough vaccine eventually. And if you get the H1N1 flu, it won’t be fun but also probably won’t do you long-term harm. In the meantime, the CDC recommends taking everyday preventative actions like hand washing and avoiding contact with sick people. (And if you get sick, please stay home.)

Is the vaccine safe?

The H1N1 vaccine is made the same way as the seasonal flu vaccine. The manufacturers just tweaked the recipe with the new virus. The Food and Drug Administration approved the vaccine in September. People with allergies to chicken eggs, however, should not be vaccinated as eggs are used to make the vaccine.

I got a seasonal flu vaccine last month. Why won’t that work against H1N1?

For the same reason that your flu vaccine from last year doesn’t protect you from this year’s seasonal flu: There are many different types of flu virus, and they mutate over time. When you are exposed to one type, your body’s immune system learns to protect you from that type only. The others are too different to register with your immune system as the same virus.

I’ve heard that in other countries the vaccine contains squalene. What is it and why is it in their vaccine and not ours? And what about thimerosal?

Squalene is a type of naturally-occurring oil found in plants and animals (including humans). Squalene is a component of some adjuvants of vaccines. Adjuvants help a vaccine’s effectiveness by boosting the immune response. Some countries have added the squalene-containing adjuvant to their vaccine mix for H1N1 because it causes a lower dose of vaccine to be effective; that is, it will allow people to get more doses out of the same batch of vaccine. The World Health Organization has found no evidence of any adverse events in vaccines containing the squalene adjuvant.

The United States government chose not to use any adjuvants in the H1N1 mix in this country. However, some formulations of the vaccine do contain thimerosal, a mercury-based preservative that has been used in vaccines for decades. Getting mercury injected into your body may sound a little scary. But concerns about safety of thimerosal are unfounded. Some parents worry that thimerosal may cause autism in young children, but there is no evidence of this. Several studies in recent years have examined the possibility, but no association has ever been found.

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In light of President Obama’s declaration that the outbreak of the H1N1 virus is a national emergency, Surprising Science is setting this week aside to discuss the history and science of vaccines and their importance in battling diseases, including swine flu. See Monday’s post for part 1, A Brief History and How Vaccines Work, and yesterday for part 2, Success Stories.

It’s kind of startling that the idea of vaccines ever caught on. There is an amazing amount of trust needed: A person—often a complete stranger—is injecting you with a foreign substance. You have to trust that the substance is really what you’ve been told it is, that it has been sufficiently tested and is safe, and that it will work as advertised and not hurt you.

An 1802 illustration depicts Edward Jenner vaccinating a young woman. Several former patients demonstrate the effects of the vaccine—miniature cows erupt from their bodies. (Courtesy of the National Library of Medicine)

Despite this, most people trust the doctors, science and government and do get vaccinated. A small percentage, however, choose not to be vaccinated (or not to have their children vaccinated). And it’s been this way almost since Edward Jenner first began vaccinating people against smallpox (see the illustration).

Decades after Jenner’s discovery, the British government got involved in vaccination by passing a law in 1840 that provided free smallpox vaccinations to the poor. But later efforts didn’t go over so well. A 1853 law required all infants be vaccinated in the first three months of life and threatened parents who did not vaccinate their children with a fine or imprisonment. Riots soon broke out in several towns. In London, an Anti-Vaccination League was founded. In 1867, after the law was extended to children up to age 14, the Anti-Compulsory Vaccination League was founded. Opposition now focused on the law’s threat to personal liberty. (“As parliament, instead of guarding the liberty of the subject, has invaded this liberty by rendering good health a crime…parliament is deserving of public condemnation.”)

In the late 19th century, anti-vaccination movements spread across Europe and into the United States, where they succeeded in repealing compulsory vaccination laws in several western and Midwest states.

But despite the controversy, protests and pamphlets, the doctors, science and governments eradicated smallpox from the United States by 1950 and from the entire world by 1980.

Along the way, though, anti-vaccination sentiments have resulted in serious harm. For example, when the majority of the residents of Stockholm, Sweden refused vaccination for smallpox in the early 1870s, they were left vulnerable to the disease. The city experienced a major epidemic in 1874, after which vaccination was again popular.

Efforts to eradicate polio—a disease now confined to just a few countries—came off track in Nigeria due to a 2004 rumor that the vaccine “contained birth control drugs as part of a secret western plot to reduce population growth in the Muslim world.” Polio is on the rise again in Nigeria, and more than 100 children have been left paralyzed by the disease this year.

And in places like Europe, Australia and the United States, in communities where parents have stopped vaccinating their children for fear that common childhood immunization causes autism (a fear that is completely unfounded), diseases that had become rare—like measles and pertussis—are making a comeback, as Wired magazine notes in their November issue:

“I used to say that the tide would turn when children started to die. Well, children have started to die,” [pediatrician and vaccine researcher Paul] Offit says, frowning as he ticks off recent fatal cases of meningitis in unvaccinated children in Pennsylvania and Minnesota. “So now I’ve changed it to ‘when enough children start to die.’ Because obviously, we’re not there yet.”

The anti-vaccination movement ebbs and flows over time, with fear of disease fighting mistrust of doctors, science and government. Which will win? If history is any guide: neither. But doctors, science and government will all need to work together to find a way to protect public health. And then, perhaps, they will find more vaccine success stories along the way.

Tomorrow—Vaccine Week, Day 4: Swine Flu Edition

In light of President Obama’s declaration of “national emergency” imposed by the outbreak of the H1N1 virus, Surprising Science is setting this week aside to discuss the history and science of vaccines and their importance in battling viruses and diseases, including swine flu. See yesterday’s post for part 1, A Brief History and How Vaccines Work.

A sign warning of a smallpox hospital during a 1953 outbreak of the disease in Yorkshire, England (WHO photo, courtesy of the National Library of Medicine)

Smallpox: Once one of the world’s most dreaded diseases, smallpox killed as many as 30 percent of people who became infected with it and left survivors deeply scarred; no effective treatment was ever found. English physician Edward Jenner in 1796 discovered how to use cowpox virus to vaccinate individuals against smallpox. Vaccination efforts grew over the next century. The last reported case in the United States occurred in 1949, and vaccination ended here in 1971. The last case of smallpox in the world occurred in Somalia in 1977, and the disease was declared to be eradicated in 1980.

Polio: The virus mainly attacks children under the age of three, and infection can result in severe paralysis and death. Vaccines developed in the 1950s and 1960s have eliminated the disease from much of the world. However, cases are still found in several countries, and immunization efforts continue in Africa and Asia.

Measles: Measles is a respiratory disease that is accompanied by a rash. In the United States and other countries where measles vaccination is common, incidence of the disease has become rare, which is good because it can lead to pneumonia, encephalitis or death. Worldwide, there are about 10 million cases of measles each year and 197,000 deaths. But if there were no vaccinations, the World Health Organization has estimated that 2.7 million people would die of the disease each year.

Hib meningitis: The bacterium Haemophilus influenzae type b causes meningitis and pneumonia. It used to be the leading cause of bacterial meningitis in children. However, since the development of vaccines for the disease in the 1990s, it has been nearly eliminated in industrialized nations. The story isn’t so positive in the developing world, though. There, Hib infects about three million individuals and kills about 386,000 each year, mostly children under the age of five.

Tetanus: “He stepped on a rusty nail and died” was once a common epitaph. Tetanus, also called lockjaw, isn’t actually caused by the rust; it’s caused by the spores of the bacterium Clostridium tetani. A person becomes infected when dirt enters a wound. Babies can also become infected at birth following a delivery under non-sterile conditions. Infection results in stiffness, muscle spasms and, about a fifth of the time, coma and death. With increased rates of vaccination, though, incidence of the disease is declining worldwide.

Diphtheria: This upper respiratory tract infection is caused by the Corynebacterium diphtheriae bacterium. It has a fatality rate of about 5 to 10 percent, though that rate climbs to 20 percent among the very young and the elderly. Vaccination has driven the incidence of the disease in the United States from hundreds of thousands of cases per year in the 1920s to just a handful of cases today.

Tomorrow—Vaccine Week, Day 3: A History of Vaccine Backlash

La Vaccine, 1827 (courtesy of the National Library of Medicine)

In light of President Obama’s declaration of “national emergency” imposed by the outbreak of the H1N1 virus, Surprising Science is setting this week aside to discuss the history and science of vaccines and their importance in battling viruses and diseases, including swine flu.

More than two millennia ago in China or India, someone noticed that people who suffered and recovered from certain diseases never became reinfected. In a leap of logic, the person who noticed the connection tried to prevent the disease by inoculating themselves (or perhaps someone else) with a bit of infected matter.

That idea, now called vaccination, bumbled along through history until 1796. That’s when an English physician named Edward Jenner noticed that milkmaids rarely got smallpox, though they often had blisters from cowpox, which they caught from their cows. Jenner thought that the cowpox might prevent the women from getting smallpox. To test his idea, he took some material from the cowpox blister of a milkmaid and inoculated 8-year-old James Phipps. Six weeks later, Jenner injected young Phipps with fluid from a smallpox sore; Phipps didn’t contract smallpox.

Over the next decades, smallpox vaccination spread, and it was a common practice by the end of the 19th century. Around that time, two more vaccines were developed—by Louis Pasteur—against anthrax and rabies. The 20th century would see the development of vaccines for more than a dozen other diseases, including polio, measles and tetanus.

Long after Jenner’s first discovery, biologists would discover how vaccines work to prime our immune systems to fight off infections:

Though the original smallpox vaccine used a related virus, cowpox, most vaccines use a weakened or dead form of whatever disease they’re meant to prevent. Some of these vaccines will also include a substance called an adjuvant that boosts the effectiveness of the vaccine. (Scientists figured out the workings of alum, one type of adjuvant, last year.)

When the vaccine is injected, a person’s immune system recognizes it as a foreign substance. Immune cells called macrophages digest most of the foreign material, but they keep a portion to help the immune system remember it. These identifying molecules are called antigens, and macrophages present these antigens to white blood cells called lymphocytes (which come in two types: T cells and B cells) in the lymph nodes. A mild immune response occurs, and even after the vaccine material is destroyed, the immune system is primed for a future attack.

The next time that a microbe with those antigens enters the body, the lymphocytes are ready to quickly recognize the microbe as foreign. When that happens, B cells make antibodies that attack the invading microbe and mark it for destruction by macrophages. If the microbe does enter cells, T cells attack those infected cells and destroy them before the disease can multiply and spread. The microbe is defeated before it can get a foothold in the body, before the person gets sick.

Tomorrow–Vaccine Week, Day 2: Success Stories

Couretsy of the CDC, The complex life cycle of Opisthorchis viverrini.

In Southeast Asia, an all-too-common parasite is known to increase the incidence of bile duct cancer in infected individuals. A paper just released in PLoS Pathogens shows how this happens. Knowing the molecular pathway that leads from parasite infection to cancer will almost certainly speed up the search for a cure for this cancer, and will probably add to our understanding of cancer in general.

Cancer is, of course, a category of diseases rather than a single disease. What holds cancer together as a coherent set of conditions is the inappropriate increase of cell proliferation in some tissue or another. Cell proliferation is, of course, normal and expected at some times and places. When an organism is growing there is quite a bit of proliferation. When a wound is healing, cell division must be sped up. Therefore, mechanisms have evolved to increase the rate of cell division, and many cancers are simply this mechanism operating in an inappropriate and sometimes out of control way.

The cause of inappropriate cell proliferation can be a genetic mutation, caused in turn by the chance mutation of an already susceptible gene, or by some kind of chemical or physical irritant.

Or it can be a fluke.

A fluke is a kind of worm in the class Trematoda. There are about 20,000 species of Trematoda, and many of them are parasites that live in mollusks and vertebrates. Commonly, Trematoda spend part of their life cycle in a mollusk, then move to a vertebrate host, and then move back to the mollusk host, as they reproduce alternatively using asexual and sexual mechanisms.

Opisthorchis viverrini, also known as the Southeast Asian or Oriental liver fluke, lives in a certain genus of freshwater snails and in humans, and when it lives in humans, it seems to predispose the humans to cholangiocarcinoma, which is cancer of the bile ducts.

The research reported yesterday identified a certain protein that is very similar to a human growth hormone, but that is found in and produced by the fluke.

Scientists knew that a particular protein of a type known as granulin was produced by the fluke, and it was known that other versions of granulin cause unchecked proliferation of cells. So they isolated the gene for the fluke version of the granulin, and placed the gene in bacteria which allows the production of sufficient quantities of the protein to use in experiments. This, in turn, allowed them to test the hypothesis that this fluke-produced protein acts like other granulin molecules in causing cancer-like growth of cells.

It turns out that fluke produced granulin is an effective cancer-causing agent.

The fluke appears to use the granulin to induce cell growth for its own nutrient supply. In addition, the fluke-produced granulin induces specific antibodies in the host that neutralize the granulin. So, there seems to be something of an arms race between parasite (fluke) and host (human).

Now that the protein is both characterized and linked to the cancer, it may be possible to produce a drug that will fight it, or to refocus efforts on the fluke infection itself to reduce the prevalence of this cancer. Also, the Opisthorchis viverrini system may now serve as a useful model for the study of growth hormone induced cancers.

Another reason that this research is very important is that there were two very strong hypotheses for the prevalence of this cancer in southeast Asia. The fluke could have caused the cancer by simply irritating the cells where the fluke lives. Alternatively, the people in regions where this fluke are common also have a diet high in a particular chemical compound called nitrosamines, abundant in the fermented fish eaten in the region, and thought to be possibly cancer-causing. While this research does not rule those ideas out, it does strongly suggest that fluke-excreted granulin is the culprit that should be addressed first.

This research is published in an OpenAccess journal, so you can read the original by clicking here.

Meet the newfound hominin Ardipithecus ramidus. Credit: T. White

A 4.4-million-year-old hominin is shaking up our understanding of human evolution this morning. The first bits of the new species, called Ardipithecus ramidus, were discovered in 1994, and now (it took a while), scientists are publishing an exhaustive analysis of the hominin and the habitat in which it lived. The scientists, working in Ethiopia, found 36 individuals, including one that preserves some of the most important features for studying the evolution of human traits.

In addition to 11 scientific papers, Science is publishing a news account by Ann Gibbons, who visited the Ethiopian field camp and writes about what it took to find these fossils and make sense of them. (One piece of her story is subtitled: “How do you find priceless hominin fossils in a hostile desert? Build a strong team and obsess over the details.”)

This remarkably rare skeleton is not the oldest putative hominin, but it is by far the most complete of the earliest specimens. It includes most of the skull and teeth, as well as the pelvis, hands, and feet—parts that the authors say reveal an “intermediate” form of upright walking, considered a hallmark of hominins. “We thought Lucy was the find of the century but, in retrospect, it isn’t,” says paleoanthropologist Andrew Hill of Yale University. “It’s worth the wait.”

Ardipithecus ramidus lived more than a million years before Lucy, an Australopithecus fossil that until now was our best source of information about how humans evolved from a shared ancestor with chimps about 7 million years ago. The new fossil shows that human ancestors–even relatively shortly after this evolutionary split–were much less chimp-like than people thought. The new species walked upright, although its feet had opposable big toes that were

Illustrations of the skeleton and possible appearance of "Ardi." Courtesy of Science/JM Matternes

good for gripping as it climbed trees. It wasn’t a knuckle-dragger. Males and females were about the same size (50 kilograms). They were agile climbers. Perhaps most intriguingly, neither males nor females have the dagger-like teeth that chimps use to fight one another. Their stubby teeth suggest that they were social and cooperative. Many of the characteristics of chimps and gorillas that people thought might have been shared by early hominins instead must have evolved in the great apes after the split with our ancestors.

“What Ardipithecus tells us is that we as humans have been evolving toward what we are today for at least 6 million years,” said Owen Lovejoy of Kent State in Ohio during a press conference this morning. “It was one of the most revealing hominid fossils I could ever have imagined.”

The scientific analyses of the fossil and news stories about its discovery are available on Science’s website.