A Real Game of Thrones

August 28, 2015 by

July 31, 2015

By Medical Discovery News

The mummies of ancient Egypt have given science much insight into their lives and deaths. Just a year ago they unearthed an unknown pharaoh from a dynasty whose existence historians had only speculated. Although ancient tomb robbers had torn his mummy apart, modern archeologists have cataloged the 18 blows he suffered in battle that led to his death over 3,600 years ago.

An expedition led by archeologist Josef Wegner from the University of Pennsylvania at Abydos in Sohang Province (about 300 miles south of Cairo) discovered the tomb of Woseribre Senebkay, who lived from about 1650-1600 BC, and was probably one of the first kings of a dynasty in Abydos. The tomb consisted of four chambers, which was modest for a pharaoh, and a burial chamber made of limestone with the goddesses Nut, Nephthys, Selket, and Isis painted on the walls. The discovery confirms the existence of a separate dynasty in Abydos, which was suggested by Egyptologist K. Ryholt in 1997. It also identifies the necropolis as a site called Anubis Mountain.

Nearby, archeologists discovered another royal tomb belonging to Sobekhotep I of the 13th dynasty, who died around 1780 BC. Interestingly, Senebkay’s canopic chest, which housed jars of internal organs, was reused from this earlier king and still bore his name covered over by gilding. A 16-ton sarcophagus made of rose quartzite was also reused from an earlier era, suggesting that this dynasty had limited resources and faced pressure from larger kingdoms surrounding it: Thebes to the north and Hyksos to the south.

Archeologists were able to recover the pieces of Senebkay, reassemble his skeleton, and perform a full forensic analysis. He was about 5’10” tall and died in his 40s. He suffered 18 wounds that penetrated to the bone, including large cuts to his feet, ankles, and lower back. There were multiple skull injuries that were similar to the size and curvature of Egyptian battle axes. The scientists theorize that the pharaoh was either mounted on horseback or in a chariot when the attack occurred, so to bring him to ground his numerous assailants slashed at his legs, feet and back. Then they killed him with blows to the head.

The use of horses in battle was not common until after 1200 BC, some 350 years later, but it is thought the Egyptians might have begun using them much earlier. Indeed, examination of Senebkay’s legs and pelvis showed signs that he spent much of his time on horseback. It also appears that he was killed far from his home as his mummification happened long after his death.

What we don’t know is who killed him, whether he was battling against Hyksos rulers, Thebans, or some other group. This was a time when the central authority of Egypt collapsed, dividing the nation into many small kingdoms. However, his tomb has brought to light more of the history of these ancient people. Who knows what’s left to find, buried in the sands of Egypt.

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The Bright Side of Black Death

April 25, 2015 by

April 17, 2015

By Medical Discovery News

Bright Side of Black Death

It’s easy to think that nothing good could come from a disease that killed millions of people. But Dr. Pat Shipman, an anthropologist at Pennsylvania State University, disputed that notion in his recent article in “American Scientist,” where he suggested the Black Death that ravaged Europe in the Middle Ages may have resulted in some positive effects on the human population. Considering that we are in the midst another significant plague (the Ebola virus in West Africa), we could certainly use more information about the role of pandemics on human populations.

The Black Death or Bubonic plague started in the mid-1300s and was caused by a bacterium called Yersinia pestis, which typically enters the body through the bite of a flea. Once inside, the bacterium concentrates in our lymph glands, which swell as the bacteria grow and overwhelm the immune system, and the swollen glands, called buboes, turn black. The bacteria can make their way to the lungs and are then expelled by coughing, which infects others who breathe in the bacteria. The rapid spread of the infection and high mortality rates wiped out whole villages, causing not only death from disease but starvation as crops were not planted or harvested. It killed somewhere between 100 million to 200 million people in Europe alone, which was one-third to one-half of the entire continent’s population at the time. The plague originated in the Far East and spread due to improved trade routes between these two parts of the world.

Today, global travel is easier than ever thanks to extensive international airline networks. Just like with the Black Death, our transportation systems could enhance the spread of a modern plague. Of course, modern healthcare is also more sophisticated and effective, but as the latest Ebola outbreak has reminded us, a pandemic is a realistic possibility.

Dr. Sharon DeWitte, a biological anthropologist at the University of South Carolina, recently made several discoveries from comparing the skeletal remains of those who died from the Black Death and those who died from other causes during the same era. First, she found that older people, who were therefore already frail, died at higher rates. Killing this group at a higher rate created a strong source of natural selection, removing the weakest part of the population.

After the plague years, she found that in general people lived longer. In medieval times, living to 50 was considered old age. But the children and grandchildren of plague survivors lived longer, probably because their predecessors lived long enough to pass on advantageous genes. Today, a genetic variant in European people called the CCR5-D32 allele, which was favored during the natural selection initiated by the plague, is associated with a higher resistance to HIV/AIDS.

Microbes have an intimate relationship with human populations and have shaped human evolution through the ages. We may see survivors of the Ebola virus passing on similarly advantageous genes through natural selection as well.

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Biological Fountain of Youth

April 25, 2015 by

March 27, 2015

By Medical Discovery News

The Biological Fountain of Youth

Over 500 years ago, Ponce de Leon landed in Florida as part of his search for the fountain of youth – magical waters that reverse aging, prevent illness, and grant immortality. He never found it, and neither has anyone else. While immortality is still impossible, we have come a long way in understanding the aging process.

We do not know the precise mechanism of aging, but there are some fundamental processes in our bodies that begin to change and this can drive aging. There are several theories of aging under intense scientific investigation.

A widely accepted theory of aging today is called evolutionary senescence, which mainly hinges on the concept of mutation accumulation. As we age, our cells accumulate mutations in our genetic material or DNA, which affects the ability of our cells to replicate and our tissues to regenerate. Also, some of our genes are designed to enhance reproduction early in life, but can cause problems later. Since genes can only be passed on during reproduction, which generally occurs earlier in life, genes that have negative effects later in life are not removed from the population – we are stuck with them! A good example is a gene called p53, which controls the fate of damaged cells by preventing their replication or directing them to die. This is important in preventing cancer in young people, but it may negatively impact our ability to replace aging cells in tissues as we grow older.

Another widely discussed theory centers on the maintenance of our genomes. As we get older, we accumulate damage to our DNA, which affects cellular function and our ability to renew tissues in the body. In a sense, this is a high mileage effect. Take for example the production of free radical molecules. These highly reactive molecules are normally produced in mitochondria, which use oxygen to produce cellular energy, a process that creates free radical molecules as a by-product. These free radical molecules lead to oxidative damage of DNA and other cellular components.

There is also evidence the neuroendocrine system (hormones that affect neurological function) influences aging. For example, a reduction in hormone levels can lead to a lengthening of life, at least in experimental animals. We are beginning to suspect that the insulin-related hormonal pathway may play a significant role in aging, at least in mice. Mutations that reduce the amount of this circulating hormone extend life.

A relatively new model of aging involves the replication of chromosomes as cells divide. When cells replicate, specialized structures at the ends of chromosomes called telomeres are shortened. Shortened telomeres are linked to decreased viability and increased cancer risk. Cells whose telomeres reach a critical length can no longer divide and are described as senescent.

We are expanding our understanding of how aging occurs. The search for a modern-day fountain of youth will require a great deal of dedicated work by biomedical scientists to safely improve and extend human life.

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Humanizing the Mouse

April 25, 2015 by

March 20, 2015

By Medical Discovery News

Humanizing the Mouse

In the 1986 horror movie “The Fly,” a scientist’s teleportation experiment goes awry when a fly lands in one of the teleportation pods and he undergoes a transformation into a part fly, part human monster. Today, science has given us the capability to create animal-human hybrids, although so far none of them has craved human flesh like they tend to do in the movies.

Neuroscientists at the Massachusetts Institute of Technology (MIT) have been introducing human genes into mice to study the effects on mouse brain function and capabilities. They are doing this in small steps, using genetic engineering techniques to introduce a specific, single human gene into a mouse. This will allow scientists to evaluate the impact of each human gene on the brain in another species. It’s not quite a monstrous Franken-mouse, but the results have definitely been revealing.

The human version of gene Fox2p is connected with language and speech development, a trait associated with the higher order brain function unique to humans. When this gene was introduced into mice in the experiment, they developed more complex neurons and more extensive circuits in their brains. Scientists wondered if this gene is responsible for the enhanced brain and cognitive abilities displayed in humans.

In the behavioral experiments at MIT, scientists placed mice in a maze and evaluated the reactions of mice harboring the Fox2p gene versus normal mice. The maze offered two modes of navigation to the mice: visual clues in the environment that were observable from within the maze and tactile clues in the pathways of the maze consisting of smooth or textured floor.

The hybrid mice learned to navigate the maze quickly, finishing it three times faster than normal mice. This cognitive enhancement or flexibility reflects the human capability of handling and processing information. The tactile information is handled by something called procedural or unconscious learning. However, the sight-derived clues represent declarative learning. It is the addition of the Fox2p gene that gave mice the ability to integrate both forms of learning.

Interestingly, if the visual clues or the tactile clues were removed, the hybrid mice did no better than the normal mice at navigating the maze. This might mean that the hybrid mice only performed better when they could utilize both forms of information. This ability to switch between and consider different forms of memory (procedural and declarative) is important and may explain in part why it is so important in human speech and language development.

Humanized animals are being used in a number of scientific fields to help us understand different elements of human physiology. Expect to see more of the humanization of animals in the future, but alas for you Sci-Fi fans – a Frankenmouse is not yet on the horizon.

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2014 in review

December 29, 2014 by

The WordPress.com stats helper monkeys prepared a 2014 annual report for this blog.

Here’s an excerpt:

A San Francisco cable car holds 60 people. This blog was viewed about 1,700 times in 2014. If it were a cable car, it would take about 28 trips to carry that many people.

Click here to see the complete report.

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Bring on the Milk

June 22, 2014 by

June 20, 2014

By Medical Discovery News

Milk

Drinking milk might seem perfectly natural, but it’s actually anything but. Humans are the only species who retain the ability to digest milk after childhood, or at least some of us do. Up to half of adults worldwide don’t have the ability to break down lactose, the main sugar in milk, because their bodies stop producing the enzyme lactase after the age of five.

About 65-75 percent of the population has some degree of lactose intolerance, the most common cause for digestive issues with dairy. Lactase breaks down lactose into simpler forms of sugar that can be absorbed by the bloodstream. Without this enzyme, lactose is fermented by bacteria, causing symptoms like abdominal pain, bloating, flatulence, nausea, and diarrhea 30 minutes to two hours after eating. Populations that have long relied on unfermented milk have the lowest rate of lactose intolerance – only five percent among the Swiss.

Humans’ ability to drink milk actually began as a genetic mutation, like the superheroes of X-Men comics. According to the leading theory, 7,800 years ago humans began to move northward. Since the sun is not out as long in northern latitudes, they could not absorb enough vitamin D from sunlight and needed another source to thrive. Milk is high in vitamin D, which aids in calcium absorption. Humans adapted to this change in their diets and developed a variant of the lactase gene that allowed them to continue synthesizing the enzyme throughout their lifetimes. Since humans with the gene variant had the advantage of consuming more vitamin D, they were successful in passing that gene on to future generations.

But new research suggests that this theory is either wrong or other factors were involved. Scientists in northeastern Spain discovered well-preserved skeletons of people who lived 5,000 years ago. DNA testing revealed that none of these eight skeletons carried the genetic mutation for lactase production. Further testing also showed that these ancient humans are indeed related to modern Spaniards. Next, computer simulations determined that over 5,000 years, chance alone would not have allowed one-third their descendants to digest milk. Strong selection for this trait would have been necessary.

These scientists developed a theory that early farmers began eating fermented dairy products such as cheeses, which have lower levels of lactose. But when food was scarce, they ran out of fermented dairy products and began to consume unfermented milk as a food source. Then, those who acquired the mutated gene for lactose production would have thrived. Those without the mutation would have suffered from diarrhea, making their situation worse, perhaps even life-threatening if they were already starving.

While the need for vitamin D from milk may have been a factor in the spread of lactase persistence, these new findings show that other factors may have also been a part of the selection process that drove this mutation into the population. Now if we could only figure out a way to turn on lactase genes again during adulthood, everyone with lactose intolerance could enjoy a pain-free ice cream cone.

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First in the No. 2 Business

June 13, 2014 by

June 13, 2014

By Medical Discovery News

Antibiotic resistance among disease-causing bacteria is a growing and dangerous problem. Bacteria resistant to one or antibiotics, like Staph and Strep, are approaching catastrophic levels. Bacteria so resistant to common antibiotics that few if any drugs are available to treat them have been dubbed superbugs. One widely feared bacterium, called Clostridium difficle or C. diff for short, causes intestinal disease so severe that it can become life-threatening. It kills almost 15,000 Americans every year, mostly the elderly. Super-resistant forms of this microbe are almost impossible to treat with antibiotics. 

This bacterium produces a powerful toxin that destroys intestinal cells and can rupture small blood vessels. It also causes abnormal intestinal behavior, mainly excess water that produces diarrhea. It’s an unpleasant and painful prospect for those infected with C. diff. 

Roughly 5-15 percent of the population carries this bacterium in their digestive system naturally, but it is kept in check by the rest of the bacterial population. But an underlying disease, antibiotics, another infection, or chemotherapy can weaken bacterial systems, allowing C. diff to expand into an infection. And a super-resistant version of C. diff can be a real problem.

As gross as it may sound, fecal transplants are getting lots of attention as an option for C. diff infections. First tried in the late 1950s, the rationale for this approach is that the disease occurs because the bacterial populations are disrupted, so providing a source of normal bacteria restores the ecology of the intestine and prevents C. diff from growing. 

Where exactly does one find fecal matter for such a transplant? It’s not as if anyone wants to ask family or friends to share their poop. Actually, there are major regulatory obstacles for fecal transplants. For instance, the fecal source must test negative for disease-causing bacteria, viruses, and parasites. Basically, it’s not something anyone can find at Whole Foods or on Amazon.

So a group of enterprising graduate students at the Massachusetts Institute of Technology (MIT) who observed a friend’s struggle with C. diff formed a company to distribute safe, certified fecal matter for transplant. OpenBiome collects, tests, and distributes fecal matter like a blood bank distributes blood. Samples are certified by Food and Drug Administration (FDA) procedures, which cost about $3,000. Then they are frozen at super-cold temperatures (-112 degrees) and shipped to hospitals and physicians. Currently, the company operates as a nonprofit and only collects a shipping and processing fee for transplant material.

We already know that our normal bacterial systems, which together make up our microbiome, help protect us from skin, urogenital, and oral diseases. Changes in our microbiome may also contribute to an underlying disease like diabetes. There is still much to be discovered about these organisms that call our bodies home, especially since we house 10 times more microbes than our own cells!

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Cancer Goggles

June 6, 2014 by

June 6, 2014

By Medical Discovery News

Cutting people open and sewing them back up for a living is a pretty stressful occupation to begin with, but some surgeons have tougher jobs than others. Cancer surgeons are charged with removing all tumor cells on the first try. But tumor growth can be irregular and it can be hard to distinguish cancer cells from normal cells during an operation. Imaging techniques like MRIs and CT scans can give surgeons a road map to the tumor, but they offer only limited help once an incision has been made.

This is because these images are merely snapshots – a single frame and dimension. Even three-dimensional images can only be viewed one frame at a time. In addition, the inside of the body is dynamic and it takes a skilled surgeon to understand the orientation of tissues and the precise margins where tumor tissue ends and regular tissue begins. 

Because of this challenge, surgeons often have to remove healthy tissue to be sure all tumor cells are gone. This requires a special step: staining the removed tissue then looking at it under a microscope to identify the cells. The surgeon wants to be sure a margin of healthy tissue is removed so no tumor cells remain.

If tumor cells remain, they will grow and second operation may be necessary to remove more cancerous tissue. Again, the removal of additional healthy tissue will be necessary. But what if a surgeon could distinguish cancer cells from normal cells during surgery? It seems impossible. Each cell is microscopic, thousandths of a millimeter. Just observing cells takes special staining and high-powered optics.

But scientists at the University of Missouri and Washington University in St. Louis are working on the impossible. They are developing cancer goggles that will allow surgeons see tumor cells right in the operating room. This new technology uses LS301, a fluorescent dye combined with a short chain of amino acids called peptide, that is only absorbed by cancer cells and glows under infrared light. This dye specifically stains cells from prostrate, colon, breast, and liver cancers among others. Patients can be injected with the dye beforehand and it will last through a procedure.

These special goggles will illuminate cancer cells with LS301 using an infrared light source. A surgeon can distinguish glowing cancer cells from normal cells and observe when they are completely removed. As a result, the surgeon would not need to remove a margin of healthy tissue to be sure all cancerous tissue is gone. This may greatly improve success rates from surgeries to remove cancerous growths. 

Currently, this technique is being perfected in veterinary surgeries to guide the removal of tumors in pets and is not yet ready for use with humans. If effective, it will be a great resource for patients undergoing tumor removal surgery in the future.

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Bear-ly Understanding Diabetes

May 30, 2014 by

May 30, 2014

By Medical Discovery News

What can studying grizzly bears reveal about human diabetes?

While they are some of the largest bears on earth, Grizzly bears aren’t usually accused of being fat. Regardless, these animals are helping scientists discover new and better treatments for human obesity and diabetes.

Grizzlies spend the late summers consuming more than 50,000 calories per day. As a comparison, a moderately active 50-year-old human female is recommended 2,300. Grizzlies then hibernate for up to seven months, relying on the pounds of stored fat they accumulated before winter. While hibernating, bears do not eat, urinate, or defecate. 

Scientists wondered if all the weight and fat bears gain results in diabetes like it does in humans. Overweight people face an increased risk of type 2 diabetes, in which the body does not make enough of the hormone insulin or cells do not respond to it. Insulin helps move a type of sugar called glucose from the blood into cells, where it is used for energy and as a precursor for other molecules the body needs. If sugar levels in the blood remain elevated and the body doesn’t have enough insulin, cells are starved for energy, leading to damaged eyes, kidneys, nerves, and hearts. 

Interestingly, Grizzly bears can actually control their insulin responsiveness. When they are the fattest, they are most sensitive to insulin, thereby keeping their blood sugar levels healthy. Soon after going into hibernation, they switch to complete insulin resistance, meaning they develop type 2 diabetes. But unlike humans, their blood sugar levels remain normal. When they awaken in the spring, their insulin responsiveness is restored. Bears do this not so much to regulate their blood sugar levels as to regulate their storage and utilization of fat. So how do bears control their insulin responsiveness? And could it lead to new treatments for type 2 diabetes in humans?

PTEN is a protein that regulates cells’ sensitivity to insulin. Scientists know exactly when Grizzlies increase or decrease PTEN activity, they just don’t know how. People with a PTEN mutation have a metabolism similar to Grizzlies’.  These people have an increased risk of obesity and cancer but a decreased risk of developing type 2 diabetes because they are more sensitive to insulin.

Grizzlies have also evolved to the ability to accumulate large amounts of fat only in their adipose tissue, just below the skin so it doesn’t interfere with the rest of their bodies. In humans, on the other hand, fat can accumulate in many places like the liver, in muscles, and around other internal organs, which are all highly unhealthy places to keep fat. Bears can also have elevated levels of cholesterol without the serious consequences of cardiovascular disease.

During hibernation, the Grizzly bears’ kidneys shut down. But despite the high levels of toxins that accumulate in the blood without working kidneys, they don’t die or even suffer from it like a human would. When they wake up, their kidney function is restored with no permanent damage.

After millions of years of evolution, Grizzly bears and other animals have developed solutions for biological challenges humans still face. Studying them is a new approach that has the potential to create treatments for many human conditions.

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