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PAGE CONTENTS:

Recognizing a Stroke

Germs

Virus or Bacteria?

How Viruses Steal Your Cells

The Bacterial Zoo on You

Eradicating Malaria

Success Over Smallpox

The Deadliest Flu Ever

New Stem Cell Science

Cancer

Recognizing a Stroke*

A neurologist says that if he can get to a stroke victim within 3 hours he can totally reverse the effects of a stroke...totally. He said the trick was getting a stroke recognized, diagnosed and getting to the patient within 3 hours which is tough.

RECOGNIZING A STROKE - A true story

Susie is recouping at an incredible pace for someone with a massive stroke all because Sherry saw Susie stumble - - that is the key that isn't mentioned below -and then she asked Susie the 3 questions. So simple.- - this literally saved Susie's life - -

Some angel sent it to Suzie's friend and they did just what it said to do. Suzie failed all three so then 9-1-1was called. Even though she had normal blood pressure readings and did not appear to be a stroke as she could converse to some extent with the Paramedics they took her to the hospital right away.

Thank God for the sense to remember the "3" steps. Read and Learn!

Sometimes symptoms of a stroke are difficult to identify. Unfortunately, the lack of awareness spells disaster. The stroke victim may suffer brain damage when people nearby fail to recognize the symptoms of a stroke.

Now doctors say a bystander can recognize a stroke by asking three simple questions:

1. *Ask the individual to SMILE.

2. *Ask him or her to RAISE BOTH ARMS.

3. *Ask the person to SPEAK A SIMPLE SENTENCE (Coherently) (ie . It is sunny out today) If he or she has trouble with any of these tasks, call 9-1-1immediately and describe the symptoms to the dispatcher.

After discovering that a group of non-medical volunteers could identify facial weakness, arm weakness and speech problems, researchers urged the general public to learn the t hree questions. They presented their conclusions at the American Stroke Association's annual meeting last February.

Widespread use of this test could result in prompt diagnosis and treatment of the stroke and prevent brain damage.

A cardiologist says if everyone who gets this e-mail sends it to 10 people, you can bet that at least one life will be saved.

BE A FRIEND AND SHARE THIS ARTICLE WITH AS MANY FRIENDS AS POSSIBLE, you could save their lives.

* Thanks to my friend JMP, who forwarded this article to me in an e-mail dated 10/24/05

Germs

Let's take a closer look at germs--those malevolent little microbes that make us sick.

The idea that disease is caused by invading microbes is really rather new. It wasn't until the mid-19th century that scientists learned that "germs" could multiply inside your body and make trouble. And it wasn't until far more recently that they learned just how various that trouble can be.

In 1864, the French scientist Louis Pasteur--who succeeded in developing vaccines for anthrax and rabies--concluded that some really bad microbugs can live in the air. By 1882, Robert Koch, a German, had extended Pasteur's observation into a discovery of huge medical significance. Koch proved that tuberculosis, a scourge of the 19th century, was transmitted through a specific type of airborne bacteria.

Koch's discovery--that specific diseases are caused by specific pathogens--revolutionized medicine. He famously outlined four postulates for linking a dangerous microorganism to a given disease:

1. The microorganism can be found in the diseased animal.

2. The microorganism can be isolated from the diseased animal and grown in the lab.

3. The cultured microorganism will cause the disease when put in a healthy susceptible animal.

4. The same microorganism can be isolated from the newly infected animal.

With a few provisos, Koch's postulates still stand as a way to determine whether a specific microbe causes a given disease. For the first time in medical history, doctors had a scientifically valid "germ theory" they could use to investigate disease in the lab and diagnose people in the world.

But doctors aren't resting on their laurels. Today, some scientists believe that many diseases we now attribute to myriad causes--such as cancer and heart disease--may actually be caused by pathogens. It's "germ theory, part II," and research on stomach ulcers has paved the way for its broader acceptance.

For years, doctors blamed stomach ulcers on spicy diet, aspirin irritation, or stress. But in 1982, Australian doctors Barry Marshall and J. Robin Warren discovered that when ulcer patients with stomachs full of spiral bacteria (Helicobacter pylori) were given antibiotics, their stomach pains and ulcers disappeared.

At first, the clinical community ignored their research. So Marshall took extreme measures. In 1985, he swallowed a cocktail of spiral bacteria and proved that the bacteria do cause stomach ulcers. With antibiotics, up to 90 percent of stomach ulcers can be tamed. Even better, a simple breath test can detect the pathogen.

This kind of evidence has some doctors believing that diseases we attribute to genes or the environment are really caused by germs. For example, patients with coronary heart disease tend to have a lot of antibodies to the bacteria Chlamydia pneumoniae. Does that suggest heart patients may be battling an infection that triggered inflammation, plaque, and ultimately arterial blockage? Some doctors think so--and say that, one day, we'll pin heart attacks on a germ.

--Michael Himick and Christina Catron

Virus or Bacteria?

Viruses steal your cells. But viruses are only one kind of microbial invader. Many of history's deadliest diseases have bacterial, rather than viral, causes. Take the infamous Black Death, or bubonic plague, which wiped out a third of Europe, China, and the Islamic world in the 14th century. Or tuberculosis, an ancient airborne disease that still kills 1.6 million people per year.

Don't blame viruses for these scourges. Blame bacteria, which are another kind of "germ" entirely. Here's a quick look at the not-so-microbial difference between the two.

Compared to viruses, bacteria are big--big enough, in fact, to be attacked by viruses that target them. You can see bacteria using a science-class microscope that magnifies them a thousand times. But to look at viruses, you need an electron microscope that magnifies them a million times.

Imagine it this way. If just one of the 10 to 100 trillion cells in your body were the size of a baseball park, the average bacterium would be the size of the pitcher's mound. The average virus would be the size of the baseball.

Viruses are not cells. They're just a few strands of rogue DNA (or RNA) looking for a free ride. They lack the components required for metabolism and replication, so they have to hijack host cells and exploit their machinery to create copies of themselves.

Bacteria are self-sufficient one-celled organisms. They have a cell wall to contain their intracellular machinery, they have a metabolism of their own, and they can live inside or outside other organisms. They reproduce independently--replicating DNA, then splitting in half, so that each new cell is exactly like the parent cell. In good bacterial weather, a single bacterium can become a billion bacteria in just 10 hours.

Viruses sicken you when they seize your body's cells and make them do their reproductive bidding. Bacteria sicken you when they digest your cells as food, or secrete toxins, or replicate rapidly in a sensitive spot. Antibiotics can kill bacteria but can't stop viruses, since they work either by destroying the bacteria's cell walls or by gumming up their intracellular machinery--and viruses have neither.

Unfortunately, it's not always easy to distinguish between viral and bacterial infections, because the symptoms often feel the same (and are often self-inflicted collateral damage as your immune system returns fire). You know soon enough, though. Viral infections tend to get better after the first few days, while bacterial infections get worse over time.

--Michael Himick and Christina Catron

How Viruses Steal Your Cells

Viruses exist to nab your cells and use them for their own reproductive purposes. They have to, because a virus is nothing more than a few strands of rogue DNA (or rogue RNA, DNA's single-stranded cousin) wrapped in a protein coat to keep out the draft.

They are not cells, and they have none of the internal structures that cells use to go about the business of life, which is, generally, to make more life. No, viruses are just genetic material looking for a free ride--looking to hijack a host cell and make its machinery do the virus's bidding.

With so little to call their own, how have these biological pirates survived for so long? The answer lies in two traits that give viruses superb evolutionary advantages: superfast reproduction and genetic mutations.

Viruses live to reproduce. Although they must do this within host cells, once inside, viruses replicate with enough abandon to shame a rabbit. They quickly reprogram the machinery that cells use to copy their own DNA and use it to spit out copy after copy of themselves.

Genetic mutations add insult to injury. With so much reproduction going on, viruses can mutate almost as fast as they propagate. And massive mutation means that each new generation of viral invaders stands a good chance of gaining some new survival or targeting advantage.

Viruses invade all kinds of cells--plant cells, animal cells, fungi, even bacteria. Yet each virus tends to have a very specific M.O. Which cells look like likely victims to a virus depends on the unique proteins found on the virus's protein coat and the protein receptors found on the poor target cell.

Some viruses recognize the general receptors that occur on many different kinds of cells. The virus for rabies, for example, can invade so many different kinds of cells that it can span species, infecting rodents, dogs, and humans.

Other viruses are more restricted and can invade only specific kinds of cells. The common cold virus, for example, can invade only the cells lining the human upper respiratory tract. It's a picky thief.

Viral entry mechanisms are as diverse as viruses themselves, which is why viruses often elude treatment. Some enter a target cell by binding to a specific receptor and passing through the host cell membrane to the cell interior. Others don't need to enter the cell, but simply attach to the surface and use a needle-like structure to inject their DNA right in.

Once viral genes are inside, the virus begins its cycle of replication. It exploits the host cell's supplies and machinery, forcing it to copy viral genes and synthesize more viral protein coats. Then, these two components come together to form copies of the virus that emerge from the host cell.

Sometimes they "bud" off the cell, like bubbles on top of a simmering stew. At other, more violent times, copies simply fill the cell until it can hold no more. It explodes, releasing its viral hoard into the surrounding area.

Either way, the viral progeny go on to infect new cells--and the cycle starts again. Disease symptoms can and do result from this cellular damage. Most often, though, the sickness you feel is the result of your immune system's response to the foreign invader. And make no mistake, it will respond.

Your immune system's first-responders act like beat cops on patrol 24/7. If they see anything amiss while walking the body's beat, they make arrests. One kind of cellular cop, the phagocytes, will engulf strange viruses and digest them. Another kind, natural killer cells, recognizes suspect changes on the surface of infected cells and releases chemicals to disintegrate both virus and cell alike.

After spotting the infection, your body can launch a more specific and intensive attack. Proteins called antibodies surround, bind to, and neutralize viruses and other invaders in your bloodstream. Killer T cells mercilessly destroy infected cells and halt systemic infection. Both help your body remember the infection and mount a faster response to the same invader next time.

Still other players merit mention. When a cell does get infected with a virus, sometimes it manages to secrete small proteins called interferons that serve to warn neighboring cells of an imminent viral invasion. These "Paul Revere" proteins work by encouraging neighboring cells to synthesize proteins that can interfere with viral replication.

--Michael Himick and Christina Catron

The Bacterial Zoo on You

Your skin is your largest organ, the boundary between you and the world, and a key part of what makes you who you are. But, despite what you may think, you're not the only one who lives in it.

In fact, according to a new study, your skin is a microbial zoo--home to perhaps 250 species of bacteria. Researchers discovered the full extent of this microscopic menagerie in what they described as "essentially the first molecular study of the skin" and its microbial inhabitants. No need to reach for the antibacterial soap, though. Most of your bacterial borders are harmless, and some are downright helpful.

Surprised? Don't be. Bacteria turn up everywhere life does, and some places most life doesn't--from the darkest depths of the ocean to the insides of your intestines. And though the unicellular organisms are best known for causing diseases, that isn't quite fair. A few bad bugs actually give countless benign--and even beneficial--bacteria a bad rap.

"Without good bacteria," says one of the study's authors, "the body could not survive." Says another, "Our microbes are actually, in essence, a part of our body." Hard to believe? Consider this: the bacteria inside your body outnumber your own cells 10 to 1, no matter how much you scrub. Your 10 to 100 trillion cells are, on average, vastly larger than the 100 trillion to 1 quadrillion bacteria that call you home, but still.

Even familiar infection-causing bacteria like Staphylococcus aureus (pictured above) don't normally cause trouble. Microbiologists say around 25 percent of the population currently carries staph, but most people don't get sick from it. Bacteria can and do cause nasty infections and dangerous diseases, but that's hardly their defining property.

So, what is their defining property? Think back to Biology 101. One of the most basic divisions in biology is the one between eukaryotic and prokaryotic cells. Basically, a eukaryotic cell includes a nucleus that holds its DNA. A prokaryotic cell has no nucleus.

Animals, plants, and fungi are built of eukaryotic cells. Most prokaryotes, on the other hand, are unicellular organisms. And bacteria are the signature prokaryotes. In fact, "bacteria" and "prokaryote" were once nearly synonymous, until enterprising biologists identified a different class of prokaryotes called "archaea."

Still, bacteria represent one of the major branches on the tree of life. Microbiologists estimate that there are 5 nonillion different bacteria species. Nonillion? Picture a 5 with 30 zeroes after it. Maybe we're the ones infesting their world.

--Steve Sampson

Eradicating Malaria

A new report from the World Health Organization (WHO) suggests there may be a way to take the sting out of one of the world's deadliest diseases: malaria, which kills around a million people each year, most of them African children.

It's not a vaccine or a high-tech medical procedure. It's a technique that mixes insecticide with good old-fashioned mosquito nets--and adds a dash of ancient Chinese medicine.

The technique is simple. Basically, you try to make sure everyone who might be infected with malaria has two things:

insecticide-treated mosquito nets to sleep under
easy access to a cocktail of anti-malaria drugs that includes artemisinin--an ancient Chinese medicine that's recently proven a boon in beating tough strains of the disease

How powerful could such a simple 1-2 punch be? According to the WHO report, the technique has already slashed national malaria mortality rates by more than half in Rwanda and Ethiopia--and they just started testing it in 2006.

That has the world's leading malaria fighters buzzing. "If this is done everywhere," says WHO's malaria chief, "we can reduce the disease burden 80 to 85 percent in most African countries within 5 years." If he's right, that could literally save millions of lives.

Malaria is caused by a parasite that infects a certain type of blood-sucking mosquito. When one of those mosquitoes bites an infected person, it slurps up tiny malaria parasites. It then injects those parasites, along with its saliva, into the next person it bites. Before long, that person is suffering fever, chills, and flu-like symptoms--if not worse--and lies ready to pass the infection along to another hungry mosquito.

Malaria parasites can also spread through blood transfusions, organ transplants, and other direct blood exchanges. But those cases are rare. Most malaria is mosquito borne--and that means you can fight the disease either by attacking the parasites that cause it or by squashing the skeeters that spread those parasites.

The new technique tries to do both. The insecticide-laced mosquito nets help prevent the nasty buggers from slurping up or spitting out new malaria parasites. Meanwhile, the drug cocktails attack the parasites within infected people.

Unfortunately, the new technique does not cure malaria. Still, according to the former director of the Global Fund to Fight AIDS, Tuberculosis, and Malaria, "This is not theoretical. We do not have to wait for a vaccine or new drugs. If we implement today's technologies aggressively on a national scale, we will have a big impact."

--Steve Sampson

Success Over Smallpox

Vaccines are variants or derivatives of pathogenic microbes that cause the immune system to mount defenses to the pathogen itself. They've been so successful in boosting the body's defensive powers that they've virtually wiped out one of the greatest scourges humans have ever known: smallpox.

In the late 18th century, English physician Edward Jenner became fascinated by a milkmaid's assertion that she wouldn't get smallpox because she had been exposed to a milder version of the disease: cowpox (the word "vaccine" comes from vacca, the Latin word for cow). So, in 1796, Jenner scratched an 8-year-old boy with a needle containing fluid from the sore of a milkmaid with cowpox. When exposed to smallpox, the boy did not come down with the disease.

The exposure to cowpox had caused the boy's immune system to form antibodies. Later, when faced with smallpox, his immune system "remembered" the pathogen and mounted a faster, more intense immune response.

It's no exaggeration to say that the smallpox vaccine is one of humanity's greatest achievements. In the 20th century alone, smallpox killed more than 300 million people, three times as many as were killed in all the wars of that century combined. Prior to that, the disease killed untold millions, slaughtering kings and commoners alike and changing the course of history again and again.

For example, the Spanish conquistadors' greatest weapon against the indigenous people of Mexico wasn't the musket or the cannon--it was the smallpox virus they carried. Exposed to a disease their immune system had never seen, the Aztecs died in droves. Today, the smallpox virus exists only in Russian and American labs. The last natural case occurred in 1977, on the heels of a worldwide immunization drive.

Most vaccines still work the same way as the one that eradicated smallpox. They use live but greatly weakened versions of pathogens to give you a mild infection akin to the serious infection you really don't want to get. Your immune system's response to the mild infection arms it with the antibody ammunition it needs to seek out and destroy the more serious infection later.

Sometimes it doesn't work--the vaccine doesn't stimulate enough of a response to do a body good. Very, very rarely, it backfires--the live pathogen in the vaccine triggers big trouble by itself. But "live attenuated vaccines" remain the only medical defense there is for many diseases, especially viral ones, since viruses are immune to antibiotics.

Other kinds of vaccines try to limit exposure to live pathogens by using pathogens that have been killed by chemicals, or by using pieces of pathogens--just the fragments needed to elicit your immune system's response. Because these vaccines don't contain live invaders, they don't cause even minor infection. Yet they're also less effective in stimulating your body's antibody production and tend to require booster shots.

Still other vaccines, called toxoids, don't use live pathogens, dead pathogens, or even pathogen pieces. They use toxins from bacteria. For example, a tetanus shot contains toxins secreted by the bacteria that cause tetanus. Once this poison is scientifically stripped of its toxic power, and becomes a toxoid, it can help your body build the antibodies it needs to neutralize terrible tetanus toxins in you.

Scientists continue to develop new vaccines. Chickenpox, caused by the varicella-zoster virus, used to be a rite of passage for children in United States. Yet since 1995, there's been a vaccine against the highly contagious disease. Made from a live attenuated virus, the vaccine prevents chickenpox in 90 percent of patients. The few kids that do get chickenpox now tend to have mild cases.

Still, viruses and bacteria evolve and mutate as fast as scientists discover ways to thwart them, if not faster. HIV, the virus that causes AIDS, has infected more than 60 million people since scientists first began noticing its devastating effects. In some countries, more than 30 percent of the adult population now carries the virus. Other deadly diseases, such as Ebola, are evolving, too. The war continues.

--Michael Himick and Christina Catron

The Deadliest Flu Ever

Most cases of flu aren't serious. But complications from the disease still claim around 36,000 lives each year in the United States alone. Worldwide, the number is ten times that. And some strains are far worse than others. Just how bad can flu get? Today, let's turn the clock back 90 years and see the flu at its all-time worst.

In 1918 and 1919, more than a fifth of the world's population caught the flu. And not just any flu--the deadliest flu ever, which caused one of the worst pandemics in history. Before it was over, between 1 and 3 percent of the world's people had perished. That's at least 20 million people worldwide.

Military bases served as incubators for the virus, in America and Europe especially. In fact, a huge number of casualties in World War I came from the flu, rather than from enemy fire. Within months, following troop movements and trade routes, the virus had traveled around the world.

The illness was so fast and so deadly that doctors couldn't believe it was influenza. It wasn't like any flu they had ever seen before. A patient who started to feel under the weather on Monday was often dead by Wednesday. Many patients turned a blue-gray hue, as fluid built up in their lungs. "It is only a matter of a few hours then until death comes, and it is simply a struggle for air until they suffocate," reported a doctor at a military base near Boston. "It is horrible."

Even worse, this virus devastated people for whom flu is normally just an inconvenience. Healthy men and women in their twenties, thirties, and forties were dropping dead on the street on their way to work or the market. How could this be the flu? Some even speculated it was a plot by the Germans, or a side effect of the mustard gas used during World War I.

But it was the flu--a horrible new strain, but just the flu. Every few decades, the flu virus, which mutates at least a little bit every year, undergoes a dramatic change. This new virus is especially dangerous because no one has built up an immunity to it. The virus of 1918-19, from the time it likely got started in Asia, was of this sort: different enough from previous strains that few people were immune.

Because flu spreads through the air, it was also frighteningly easy to get infected. All you had to do was breathe the air that a sick person had just coughed or sneezed into. The most dangerous place you could be was in a crowd.

Unfortunately, it was hard to avoid crowds in 1918. Hundreds of thousands of soldiers were being packed into barracks and onto troop ships. And huge military parades and war-bond rallies helped the virus make the leap from soldiers to the civilian population.

By autumn of 1918, life in big cities had become nightmarish. In one month--October 1918--nearly 200,000 Americans died from flu. Medical care was hard to come by, because so many doctors and nurses had been dispatched to Europe to care for the troops (and because many of those who stayed got sick, too). Churches, theaters, and taverns closed. In some cities, even funerals were limited to 15 minutes.

When one person in a family got sick, the flu usually spread to everyone else in the house. Volunteer nurses, arriving with broth and clean sheets, were seen as saviors by people too ill or too poor to get to a doctor. "In some cases," a New York City nurse wrote, "the nurses were even locked in the house by the patient's friends, or kidnapped on their rounds, so panic-stricken had people become."

The East Coast was ravaged in September 1918, and it took only a few weeks for the epidemic to spread to the West. In San Francisco and Seattle, wearing gauze masks was required by law. In Prescott, Arizona, the town council made it illegal to shake hands. Other towns quarantined themselves, forbidding trains from stopping, only to fall ill when they welcomed the postman. On the playground, children had a new jump-rope rhyme:

I had a little bird, and its name was Enza
I opened the window, and in-flew-Enza.

By the time it had run its course, the 1918-19 flu had killed more than half a million Americans. Beyond the United States, the death toll was even more appalling. What Americans called the "Spanish flu" (incorrectly thinking that was where it started) cropped up all over the world.

Germany, France, and the United Kingdom each lost at least 200,000 civilians between June 1918 and May 1919. More than half a million Italians died. In poorer and more densely populated areas, the death toll was catastrophic. In parts of Mexico, more than 10 percent of the population perished. On South Pacific islands, more than 20 percent did. In India, at least 12 million people died from flu.

The death toll for the whole world is difficult to know, but the most conservative estimate is that 20 million people died. Many researchers double that number, and some go so far as to say that the death toll could have reached 50 million.

The 1918-19 pandemic was extreme, but not unprecedented. The World Health Organization has records showing that there have been 31 documented influenza pandemics since 1580, most recently in 1968-69. And medical experts say we're overdue for another devastating flu.

--Colleen Kelly

New Stem Cell Science

We may soon be able to remove stem cell research from the list of controversial scientific quests. Two teams of scientists reported that they have used a new technique--"direct reprogramming"--to turn ordinary skin cells into stem cells with the "pluripotency" previously seen only in embryonic stem cells, without needing to create or destroy a human embryo in the process.

In other words, they've created the kind of stem cells researchers have long believed hold huge medical promise without tripping the ethical wires that have made previous stem cell research so controversial.

There is still a ways to go before the new technique is ready for medical primetime. But ethicists are thrilled, the White House is "very pleased," and one stem cell science pioneer calls it "the biological equivalent of the Wright Brothers' first airplane." To see why, let's review some stem cell science.

First, imagine you're a stem cell. As cells go, you're not very sexy. Your cellular chums even call you "generic." You don't secrete hormones, form protective layers, digest food, or otherwise perform an immediately productive role in the body. But that doesn't mean you're a freeloader.

Like little factories, you and the rest of the stem cell clan produce all of the 220 types of cells that do the jobs that keep people alive. Without stem cells like you, embryos couldn't develop, and adults, unable to replenish blood and tissue, would soon die. Not bad for a generic little cell.

In fact, generic little stem cells shape everyone's cellular destiny. Every human begins as a single cell, the zygote. Almost immediately after its creation, the zygote begins to divide, in a process called mitosis. This process will repeat over and over throughout embryonic development, infancy, and childhood. It will slow down a little for adults, but it will never stop. The end result is a human body made up of 10 to 100 trillion cells.

This amazing cell division usually works like a biological Xerox, making copy after copy of the original cell. Yet in some cases, a biological fine-tuning occurs, whereby the dividing cell--a stem cell--doesn't make copies of itself but instead gives rise to a different-looking cell that performs some specialized function. This differentiation is what keeps us from growing into 4-foot-wide basketballs of undifferentiated flesh, and stem cells make it happen.

No one knows exactly how stem cells pull off this neat trick. When specialized cells--skin cells, muscle cells, bone cells, and others--divide, they give rise only to cells like themselves. They just can't differentiate into other cell types. They generally do contain a full set of DNA, coding a complete you. Yet specialized cells express only some of the genetic information they contain, just what they need to perform their specific job.

Scientists recognize three different types of stem cells: totipotent, pluripotent, and multipotent. Totipotent stem cells, as the name suggests, have total potential--the ability, given the right conditions, to grow into a complete person. If one of these cells splits off from another, it can grow into a fully formed, separate, but genetically identical twin. Such cells exist only for a few short days after conception. After that, the totipotent cells will have divided into somewhat specialized cells that can't produce a person on their own.

These somewhat specialized cells fall into the second stem cell category: pluripotent cells. Pluripotent stem cells exist in the inner layer of a small ball of about 100 cells called a blastocyst. They can grow to become the hands, feet, digestive system, and other complex parts of the human body. Yet like totipotent cells, pluripotent cells don't last long. As cell differentiation continues, they give way to the last stem cell type: multipotent.

Multipotent stem cells are further specialized cells that can grow into only a few cell types. For example, multipotent cells in your bone marrow continually make red blood cells, white blood cells, and platelets. Although multipotent cells have lost most of their ability to differentiate into various cell types, they do have one distinct advantage. They exist throughout life, replenishing the cells you need to live.

Scientists have known about stem cells, and their role in embryonic development, for some time. But no one realized how useful they might be until 1998, when a team of researchers led by James Thomson at the University of Wisconsin successfully cultured human embryonic stem cells in the lab. Not only that, Thomson's team maintained the cultured cells in a pluripotent state, preserving their ability to become many other cell types.

Scientists have been working to build on this breakthrough in all sorts of ways ever since, using either embryonic or adult stem cells. Adult stem cell research uses multipotent stem cells that researchers can extract from practically anyone. Embryonic stem cell research uses the pluripotent stem cells of embryonic development. Researchers obtain these from the inner layer of a blastocyst, in a process that destroys the embryo. It's this process that has sparked most of the debate on stem cells, since many people regard destroying an embryo as killing a human being.

Research into the benefits of adult stem cells has produced positive results. But because embryonic stem cells can give rise to the greatest variety of cell types, most experts have maintained that they hold the greatest hope for medicine. Soon, thanks to the new "direct reprogramming" technique, it may be possible to create stem cells with the potency of embryonic stem cells without destroying embryos. That's what has ethicists and scientists alike so excited.

No one knows what future stem cell research will reveal. Yet many researchers have seen enough to think that stem cells might revolutionize medicine. They hold out hope that paralyzed people might walk, that the blind might see, or that lifetime diabetics might never again need insulin needles. Stem cell science is still just getting started--and the biggest ethical debate over it may be about to end.

--Christopher Call

Cancer

For far too many people, that diagnosis--"cancer"--strikes far too close to home. It's a disease that many of us know personally. But we still don't know enough.

Your life depends on teamwork. You probably think of yourself as one creature, but you're actually a collection of trillions of living cells, each with a specific job to do and all working to keep the rest--and hence you--alive.

Cancer cells don't work for the team. In fact, they hurt it. They divide too much, splitting wildly into new cells faster than the normal cells around them. And they don't stop dividing, regardless of the damage they cause. They simply ignore the biological cues that tell your cells when to stop.

Eventually, this unchecked cell growth can lead to a tumor--a semiautonomous mass of tissue that serves no productive purpose and that may, through its growth, damage surrounding cells. Worse still, unlike normal cells, a cancer cell can detach from its neighbors and travel to other parts of your body, causing even more damage someplace else.

The worse the cancer gets, the more the cancer cells tend to take an undifferentiated, "immature" form. Your body contains 220 different types of cells, each with a specific job to do and a form that follows that function. Cancer cells, however, are both incapable of doing a useful job and increasingly aggressive.

Cancer cells get this way because they're broken. Your cells work by following specific instructions. These instructions are found in each cell's nucleus, laid out in sequences of DNA called genes. Each of your genes--and there are tens of thousands of them--contains a code that tells a cell how to do a specific job.

At least two of these gene types, proto-oncogenes and tumor suppressor genes, can cause serious trouble if they get messed up, or mutate. Proto-oncogenes regulate when, how, and how much your cells divide. Tumor suppressor genes help keep this process in line and can put the brakes on cellular reproduction if necessary. They're also the genes that tell your cells how to fix damaged genes.

With an unlucky mutation or two, proto-oncogenes can turn into oncogenes (basically, genes that cause cancer). The affected cell becomes hyperactive, and divides free of the usual constraints. Fortunately, your tumor suppressor genes can still slam on the brakes, repair the DNA, or call for the ultimate sacrifice: apoptosis, or "cell suicide." When a cell's DNA sustains so much damage that it is beyond repair, a healthy cell still thinking of the team can destroy itself to prevent greater problems.

But if genetic errors prevent your tumor suppressor genes from doing their job, too, troublemaking oncogenes are more likely to cause cancer. And that's why cancer tends to strike older people. It takes more than one genetic mutation to make a cancer cell, and those mutations can take a long time to occur. (Unfortunately, some people are born with some mutations already.)

There are almost as many ways in which genes can go bad as there are genes involved in cancer. Molecular mutations can change your DNA sequence, scrambling the code and turning healthy genes into oncogenes. Or, errors in cell division can cause entire genes to move to a new location, get repeated, or be deleted altogether.

Sometimes, these mutations are hereditary. Other times, they happen over your own lifetime. They could be random genetic accidents, or caused by environmental exposure to carcinogens, like cigarette smoke and the UV radiation in sunlight. Even certain viral infections can lead to cancer.

In fact, part of what makes cancer so tough to cure is that it isn't a single disease with a single cause. The word "cancer" actually covers more than 100 distinct diseases, all characterized by out-of-control cell growth. Because the diseases are different, treatments that are effective for one aren't necessarily effective for others. The weapon we need to kill cancer once and for all may be an entire arsenal.

--Christopher Call

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