Lost in the Outback

The Olympic Games in Sydney are turning the world’s eyes on a continent that seems strange and mysterious to many people. Even to native Australians, the land holds stunning surprises. Only recently did they learn about the existence of one of the most amazing landscapes in the world: the Bungle Bungle Range.

The Bungle Bungles is a place where thousands of colorful rock formations shaped like beehives and striped like tigers rise in tiers. The result is a mountain range that looks like no other.

Somehow, this place managed to remain a literal blank spot on the Australian map until the 1980s. Before that, only a group of local Aborigines and a small number of other Australians knew about it.

REMOTE SECRET

To see the Bungle Bungles for myself, I joined a safari outfit on a journey to Purnululu National Park, deep in the Aussie Outback. It began in Kununurra, a town about 250 kilometers (155 miles) by road north of the Bungles.

My trip to the Bungles showed me why they had escaped widespread notice for so long. The Bungles are surrounded by many square kilometers of rugged country, which discouraged exploration. Even people who got close could have easily missed the beehives because the rolling landscape hides them from view. “You could be 10 miles away and not really know what was in there,” said Robert Young, a senior research fellow in the School of Geosciences at the University of Wollongong.

On my visit, we camped beside Picaninny Creek, a stream that emerges from the southern end of the massif(mountain mass). After setting up my tent, I gazed out at the vista I had come many bumpy miles in a four-wheel-drive vehicle to see: a seemingly endless expanse of beehive-shaped formations carved out of sandstone. Most astounding to me were the horizontal layers of orange and black that looked for all the world like tiger stripes.

DISSOLVED CEMENT

According to Young, the rock of the Bungle Bungles began forming 400 million years ago. Streams and rivers laid down layers of sand in a growing pile that eventually might have reached several thousand feet thick. The enormous pressure from all that material slowly turned the sand into sandstone. And there it lay for many millions of years, buried by even newer rock layers deposited on top.

Later, erosion gradually stripped away the overlying rock, exposing the sandstone about 20 million years ago. Streams then began cutting into the rock–the start of the process that would create the “beehives.”

Why did the sandstone erode into such unusual shapes? To find out, Young used an electron microscope to peer between the tiny quartz grains in the sandstone. Quartz is a tough, crystalline mineral made of silicon dioxide (Si[O.sub.2]). In sandstone, the quartz grains that form most of the rock are held together by a kind of cement. In the case of the Bungle Bungles sandstone, that cement consists of a compound called silica. Like quartz itself, the silica cement is also made from Si[O.sub.2].

Examining the Bungles’ quartz grains, Young determined that rainwater seeping into the rock had slowly dissolved most of the silica cement between the quartz grains. At that point, only the tightly interlocking shapes of the quartz grains themselves held the rock together.

The lack of cement makes the rock very friable; it crumbles easily under foot. But the interlocking grains make the rock strong in compression, which means that it can maintain tall vertical cliffs without falling down. The result is rock that can be carved easily by streams but that stands up in tall towers and beehives and in long, thin ridges.

BANDS OF ALGAE

There’s more to the mystique of the Bungle Bungle Range than the shape of its rock formations. Equally alluring is the orange-and-black tiger striping.

The colors, it turns out, are only skin deep; the actual sandstone is a cream color. The coating is silica cement that has leached out of the rock to form a hard veneer. Small amounts of clay and iron in the silica veneer give the beehives their orange color.

The dark tiger stripes come from algae, simple plants that live in the water or in moist places on land. The algae snuggle into tiny holes and crevices within the coarsest bands of the Bungle Bungles sandstone.

As I gazed at the striped formations during a hike into Picaninny Gorge, I wasn’t thinking of geological details. I was simply overwhelmed by the grandeur of this Outback wilderness. And as I walked up the canyon, my amazement only increased. The beehive formations gave way to cliffs, and the canyon snaked in broad S-curves as it penetrated deeper into the Bungle Bungle Range. The environment seemed to capture the essence of Australia: isolated, empty, breathtakingly luminous, and wondrously strange.

MIND GAMES

Sports are as much a mental game as a physical one. Here’s what scientists know about one key skill–reorienting.

Have you got what it takes to become an Olympic contender? Take this simple test. Hold out a hand. Position the tips of your thumb and middle finger so that a half-inch space exists between them. Then ask a friend to hold the end of a ruler so that the 1-inch mark hangs between the two fingertips. Have your friend drop the ruler without warning. Catch the ruler as fast as you can between your two fingertips. Note the number on the ruler where you caught it. Now switch roles and note where your friend catches the ruler. The person with the lower number has the faster reaction time.

Was yours the faster time? Then you must have more of what makes a great athlete, right? Wrong! Scientific studies have shown that great athletes don’t react more quickly than anyone else does. Muhammad Ali, the champion boxer and Olympic gold medalist who bragged that he could “float like a butterfly and sting like a bee,” had only an average reaction time.

Athletic success, it seems, is determined by something other than last reflexes. That “something” is the ability to act–and not act–on what you see, according to new studies.

LOOKING VERSUS SEEING

Imagine yourself dribbling a basketball down a court. What do you see before you? On the left stands the power forward, posted up close to the basket. Directly ahead, the shooting guard is spotting up on the perimeter. To the right, another forward is keeping an opponent out of the paint. Behind that forward, another teammate is moving toward the basket for a rebound. And so on.

All that visual information strikes your retinas–the layers of tiny, light-sensitive cells at the back of each eye–at the same time. From there, the information travels via the optic nerve to the brain.

So much visual data coming at you all at once might be too much to handle, except that the brain does an expert job at editing. It focuses on just one piece of information in your entire field of view at any one time. That act of focusing is what psychologists called attention.

Human attention is so focused that the mind is unaware of many things that the eyes happen to be looking at. In one lab experiment, subjects followed the movements of bouncing balls on a video screen. When the subjects were asked later if they had seen a gorilla moving around the screen, most said no. Their attention to the bouncing balls made them totally “blind” to the gorilla. That “blindness” is called change blindness, according to James Enns, a professor of psychology at the University of British Columbia.

Change blindness is the cause of many car accidents, said Enns. Numerous reports have described drivers plowing into pedestrians or even trains right in front of them. “The drivers looked, but they didn’t see,” said Enns. “Their attention had been focused on something in their field of view other than what they were looking straight at.”

ELITE VERSUS AVERAGE

So what does visual attention have to do with sports? To find out, Enns tested young hockey players who had different playing skills. What Enns found was that the elite players were much better than the average players at reorienting. They could switch their visual attention from one thing to another more quickly and with greater accuracy.

“Hockey players need to monitor a whole bunch of different things on the ice,” said Enns. “The highly skilled players were the ones who were better at responding–or not responding–to all the different things happening in their environment.”

Superior visual attention might have been what National Hockey League goalie Mike Liut was referring to when he was interviewed once about hockey megastar Wayne Gretzky. “I’d see him come down the ice and immediately start thinking, ‘What don’t I see that Wayne’s seeing right now?'” said Liut.

CLOSED VERSUS OPEN

Not every sport requires superior reorienting, says Enns. Such ability is necessary only for what Enns calls open-skill sports–those in which the athlete has a wide field of visual information. Volleyball, soccer, basketball, and tennis are some open-skill sports.

Enns labels sports that don’t have a wide field of visual information closed-skill sports. Swimming and sprinting are two examples. The best closed-skill athletes are those who can focus their attention on one location in space and block out all other distractions that might otherwise slow them down.

NATURE VERSUS NURTURE

Enns doesn’t know whether the best open-skill athletes are born with a superior ability to reorient or whether that ability comes with practice. “All we know at the moment is that there is a link between their sports skills and their skill at reorienting,” he said.

WHAT DO YOU SEE?

Examine these two photographs.

  • How are they different?
  • How long does it take you to find the difference?
  • Why is this a test of visual attention?
  • Why might some people take longer to find the difference than others?

The Real Dopes?

In their quest for success, many athletes are abusing science by taking banned drugs.

During the 1997 Tour de France bike race, officials tapped French cyclist Erwan Mentheour (at right) for a random drug test. Just before the race, Mentheour had taken erythropoietin (EPO), a performance-enhancing drug banned in the 2,400-mile race.

One side effect of EPO is that it thickens the blood. So Mentheour’s trainer and doctor tried thinning his blood before the test. They injected him with sugar. Then they bled him. Mentheour still tested positive and was thrown off the racing circuit.

Within two weeks, Mentheour was allowed back on his bike. He claimed his blood had been out of whack because he had had diarrhea and had lost a lot of water. The truth, he later confessed, was that he’d been taking EPO and other banned performance-enhancing drugs. “That was part of the job,” he said.

Mentheour is far from alone. Many other athletes have confessed to, or been caught, taking forbidden drugs. All of them had put science to dark purposes: winning at all costs.

PITUITARY POWER

Probably the most popular performance-enhancing drug at the moment is human growth hormone (hGH), which is also banned in most sports. The drug hGH is a synthetic form of a hormone made naturally by the pituitary, a pea-sized gland attached to the base of the brain. Natural human growth hormone has a profound effect on every cell in the body. It helps young people grow tall and strong. It slows down the aging process in older people. Some doctors call it the “fountain of youth.”

Scientists developed hGH in the 1980s to treat dwarfism, a form of stunted growth. In 1996, the U.S. government also approved hGH for use in adult patients suffering from human growth hormone deficiencies, usually caused by pituitary diseases or infections. To their surprise, the patients found themselves developing bigger, stronger muscles.

That news prompted many athletes to get hold of hGH on the black market and start taking it. Among Olympic athletes, hGH use became so widespread that Charles Yesalis, a professor at Penn State University, called the 1996 Olympics in Atlanta the “growth hormone Games.”

BIG BONES

According to Yesalis, hGH helps athletes train harder and longer and recover faster after training. However, the side effects can range from severe bloating to excessive bone growth in the face, hands, and feet. “There are rumors about bodybuilders who have used hGH and grown one or two shoe sizes,” said Yesalis.

The long-term effects of hGH are still unknown. But Lyle Alzado, a former lineman for the Los Angeles Raiders football team, believed that the brain cancer that eventually killed him was caused by his use of hGH and steroids, another banned drug.

Although hGH is banned in most sports, no approved test for it exists. Testing for hGH is difficult because it so closely resembles natural human growth hormone. Strenuous exercise also increases natural human growth hormone production, and people vary widely in their natural hormone levels.

Scientists are working on a blood test that identifies the presence of hGH in the body. However, until that test proves reliable enough to stand up in court, the International Olympic Committee (IOC) will not begin testing at the Olympics.

EPO DEATHS

Another popular performance enhancing drug is synthetic EPO, the drug cyclist Erwan Mentheour was caught taking. Natural EPO is a hormone produced by the kidneys when oxygen levels in the body’s tissues drop. EPO commands the body to make more red blood cells, which carry oxygen to the body’s cells.

Synthetic EPO was developed in the late 1980s to fight anemia, a condition marked by extreme paleness and fatigue and caused by a low red blood cell count. Shortly after, endurance athletes discovered that synthetic EPO could help them turn in superhuman performances. The extra red blood cells carry extra oxygen, boosting athletes’ endurance.

The side effects of EPO include muscle tremors, oily skin, acne, and skin flushed by the heart’s effort to pump blood made thick from too many red cells. Extreme side effects include high blood pressure, heart attacks, and strokes. Since 1987, EPO abuse has reportedly killed about 20 cyclists.

One test for EPO, called a hematocrit test, already exists–the same test that busted Mentheour in 1997. The IOC won’t use the hematocrit test because it doesn’t actually detect EPO. It only reveals how many red cells are in the blood.

Last month, however, the IOC announced that it would administer two new tests that detect synthetic EPO in urine and blood samples. Many applauded the decision. Yesalis and other critics said, however, that the use of other banned substances has grown worse since the Atlanta Games. The new EPO tests won’t stop this month’s competition from being the “most-doped Games,” said Yesalis.

At least, the Sydney Games won’t be known as the “hGH-EPO Games.”

Master Gland

The pituitary gland, pictured at right, is the most important gland in the body. It releases at least nine hormones. Some of those hormones have direct effects on the human body. Others prompt different glands to release hormones of their own.

Ride like The Wind

U.S. cyclist Erin Hartwell, 31, was riding the fastest bike ever tested in a wind tunnel when he captured a silver medal at the 1996 Olympics in Atlanta. That bike was the ultra-aerodynamic Superbike II. Aerodynamics is the study of objects moving in air.

“In cycling, aerodynamics is everything,” said Sam Callan, manager of sports science for the U.S. cycling team. “If you can go 1 percent faster, it can be the difference between a gold medal and no medal.”

Yet even riding Superbike II, the team won only a few medals. The 1996 Olympics taught the U.S. team an important lesson: Bikes alone do not win medals.

Shortly after the ’96 Olympics, the world governing body of cycling set new regulations for bike construction. Those regulations took the Superbike II out of competition.

“The Olympics wants the best athletes to win, not the richest country or the country with the best technology,” said Steve Morrissey, team operations and equipment manager for the U.S. cycling team.

What made the Superbike II so different? First, the frame of a regular racing bike, from its handlebars to its wheels, is made of tubular parts. But the parts of the 16-pound Superbike II were shaped like airplane wings to reduce drag, or air resistance.

Second, the Superbike II’s handlebars were custom-made to suit each athlete’s riding position. The front wheel was smaller than the back wheel, enabling riders to sit low. In that position, the riders could save energy by taking advantage of the wind-blocking effect of the racer in front of them. Cyclists call that effect drafting.

Now that the Olympic regulations governing bike construction are stiffer, the emphasis has shifted to the “engine”–the athlete–and not the machine. If bikes can’t be made more aerodynamic, cyclists can be. Cyclists can wear one-piece skin suits made of fabrics that keep air flowing around the suits instead of through them, to reduce drag. Cyclists can also reduce drag by learning to ride like Alpine skiers, with their arms low and their backs flat.

“But they can’t [lie] out on a bicycle like Superman flying through the air,” Morrissey said. “There are rules against that.”

Cracking the Code

Scientists recently mapped you body’s blueprint for life, the human genome. Here’s what that feat means for science and for you.

Where were you June 26? That day marked a milestone in science, one that future historians may compare to the first walk on the moon or even the invention of the wheel. Scientists announced that they had prepared a rough draft of the human genome — the blueprint for human life.

“This is a spectacular achievement,” commented Richard Lifton, head of the genetics department at the Yale University School of Medicine.

Decoding the human genome (JEE-nohm), say scientists, will give them the complete operating instructions for the human body. It will also give them the knowledge that will lead, in time, to reducing or even wiping out thousands of diseases. Finally, it may even give scientists the awesome power to modify the human genome and custom-design human life.

WHAT IS A GENOME?

Decoding the human genome consumed an enormous amount of time (ten years), money ($3.5 billion), and effort. In one lab alone, robots the size of Volkswagen Beetles toiled around the clock, processing snippets of human tissue. Supercomputers in nearby rooms, running on $1 million in electricity each year, analyzed the snippets.

Why was so much work necessary? Because the human genome is the sum of all human deoxyribonucleic (dee-OK-si-righ-boh-noo-KLEE-ik) acid (DNA). DNA is an invisibly tiny substance that stores information in a living thing. In human beings, almost every cell holds an identical copy of DNA.

If you could extract the DNA from one human cell, unravel it, and examine it end-to-end, you’d see a fantastically long chain made up of 3.2 billion microscopic links! Each link is made of one of four kinds of chemicals, or nucleic acid bases: adenine (A), cytosine (C), guanine (G), and thymine (T).

When scientists announced that they had decoded the human genome, they in essence said that they had determined the order in which most of those 3.2 billion bases are linked: TCGGATATTAAG …

ONLY THE BEGINNING

Two teams of scientists broke the code, and they won’t be resting anytime soon. Their work has just begun. As they admitted in June, their work is riddled with errors–inevitable when billions of pieces of data are being handled. In addition, certain sections of the genome have yet to be fully decoded.

Even when scientists completely map the genome, they still must decipher it. And that means isolating its genes. Genes are those parts of the human genome that tell a cell what to do. Genes rule. Every cell type in your body is controlled by a different set of genes.

The human genome is thought to hold about 50,000 genes. So far, only a few of them have been named and fully analyzed.

GENE HUNT

Locating the remaining genes in the human genome will be the next task–and it won’t be an easy one. A gene can be anywhere from 1,000 to 10,000 bases long. To identify which bases make up each gene, scientists will have to sift through long stretches of bases they assume are useless, or “junk DNA.” Scientists estimate that genes make up just 3 percent of the human genome. The other 97 percent is junk DNA.

Even when the genes are separated from the junk, the job will continue. Genes are simply sets of instructions. The actual work in a cell is done by the proteins that the genes instruct the cell to make. Every chemical reaction in the body depends on proteins, of which there are as many as 2 million types. Imagine the job of finding out what all those proteins do! A whole new science of protein research, called proteomics, is just now taking off.

21st-CENTURY DILEMMAS

In the years ahead, genomic knowledge will explode. And with that explosion, scientists expect, will come ways of finding and attacking the faulty genes that cause genetic diseases. (See “Visiting the Gene Doctor,” page 6.) Eventually, brand-new types of genes might be built from scratch–genes that might endow human beings with Hulklike strength or hearts that don’t fail or bodies that don’t grow old.

Such feats will raise profound questions: Who should be permitted to tinker with the human genome? Should parents be allowed to order up genetically programmed children? Should genomic science be used to build a race of superhumans? How could we stop the building of superdestructive humans?

In the meantime, Sydney Brenner, a researcher at the Molecular Science Institute in Berkeley, Calif., estimates that each gene and its products will take a whole lifetime to study. If the human genome holds 50,000 genes, that means 50,000 lifetimes of work, or 50,000 complex, challenging jobs. Many people will one day make their mark in those jobs. Why not you?

The Coming Storms

Get ready for a couple of decades of ugly hurricanes. Here’s why.

Did that humongous wall of water in this summer’s hit movie The Perfect Storm blow your mind? Well, that’s entertainment. No wave that size was actually recorded during the real “perfect storm” in 1991.

Still, Atlantic storms can be fierce — and could be getting fiercer. Global climate change could soon whip up hurricanes unlike any ever seen before, say scientists.

MONSTER STORMS

The last several years have already been bad ones for Atlantic Ocean hurricanes. Two years ago this month, Hurricane Georges destroyed $2 billion in property in Puerto Rico. A month later, Hurricane Mitch killed 10,000 people in Central America. Then, last September, Hurricane Floyd trashed $6 billion in property on the U.S. eastern seaboard and prompted the largest evacuation (more than 3 million people) in the country’s history.

The recent upswing in storms is part of the natural up-and-down cycle of hurricane activity in the Atlantic Ocean, according to James Elsner of Florida State University. The number of big Atlantic hurricanes was relatively high form 1943 to 1964. In 1995, big hurricanes made a comeback that Elsner says could last through the next few decades.

Why does hurricane activity flip-flop? Elsner puts the blame on the thermal haline circulation, a circulation pattern that moves warm seawater from the Pacific Ocean by way of the Indian Ocean to the Atlantic Ocean, then back again.

During some periods, the thermalhaline circulation moves more quickly and makes the North Atlantic warmer than normal. Such periods prompt more hurricane activity in the Atlantic because warm water supplies the fuel–the heat energy — that keeps a hurricane going, said Elsner. (See “Anatomy of a Hurricane.”)

THE HEAT IS ON

The coming decades could be ones of not just more but also bigger ocean storms. Bigger storms could gain their extra power from global warming, the gradual rise in Earth’s surface temperature that many scientists believe has been caused by a buildup of carbon dioxide ([CO.sub.2]) in the air. Global warmlng is expected to continue well into the 21st century, making the world hotter than ever.

As the world gets warmer, so do the oceans. And warmer oceans hold more of the thermal (heat) energy that hurricanes feed on. According to Kerry Emanuel, an atmospheric scientist at the Massachusetts Institute of Technology, hurricane wind speeds increase by 5 miles per hour for every extra degree Fahrenheit of water temperature. A warmer ocean might push hurricane winds to speeds of 200 miles per hour or more. Only a few hurricanes have ever had wind speeds exceeding 155 miles per hour.

PACIFIC POOL

That’s one forecast. Some scientists say that further global warming might have an opposite effect and dampen hurricane activity. William Gray, a meteorologist at Colorado State University, says continued rises in global temperatures might produce more El Ninos. El Nino is huge pool of warm water that often develops in the Pacific Ocean. When an El Nino is in place, high-altitude winds regularly blow east to the Atlantic Ocean. Those winds can snuff out Atlantic hurricanes by essentially lopping off their tops.

Super hurricanes might fail to take shape for another reason. Scientists have noticed a tendency for Hurricanes to “commit suicide.” When a hurricane reaches a certain size, it starts stirring up cold water from deep in the ocean. Such an upwelling of cold water can rob a hurricane of its energy and kill it. Any supersize storms that arise due to global warming might also die out quickly from exposure to the cold.

STORM WARNINGS

Whatever global warming brings, scientists agree on the need for better hurricane forecasts. One scientist, Isaac Ginis of the University of Rhode Island, has devised a new way of assessing the strength of hurricanes. Ginis’s technique focuses on the thermocline, a narrow zone of water that underlies the ocean’s warm surface water. Beneath the thermocline, the ocean turns very cold.

As mentioned, hurricanes weaken and die when warm surface water mixes with the cold water below. That mixing is partly determined by the depth of the thermocline. The shallower the thermocline, the more likely the hurricane will stir cold water up to the surface.

Last year, Ginis and colleagues measured the depth of the thermocline over the entire North Atlantic. Their measurements helped them improve predictions of hurricane strength by about 30 percent, said Ginis.

Ginis’s forecasting method could prove to be a major lifesaver. If history is any guide, the current surge in hurricane activity could last at least 20 more years.

Anatomy of a Hurricane

  1. A hurricane forms where humid air flows over warm ocean water. The air, warmed by the ocean, begins to rise.
  2. When the rising humid air reaches a certain altitude, the water vapor in it condenses and forms walls of huge cumulonimbus clouds, called rainbands.
  3. The condensation of water vapor also releases a huge amount of heat energy. That energy fuels the hurricane, making it grow in size and shape.
  4. The spiraling motion of a hurricane is caused by the Coriolus effect, a turning of the wind produced by Earth’s rotation.

A tropical storm is classified as a hurricane when its winds reach 117 kilometers (73 miles) per hour. The average hurricane is 480 kilometers (300 miles) wide and lasts about ten days.

 

Visiting the Gene Doctor

Tanisha Daniels, 12, is a happy, energetic girl who likes going to the mall and gabbing on the phone–when she’s not sick.

Tanisha has sickle-cell anemia, a disease that causes normally round red blood cells to become sickle-, or crescent-, shaped. Sickle-shaped cells clog blood vessels, causing fatigue and attacks of intense pain, often referred to as pain crises. “The pain that is inflicted on my body when I am in a pain crisis is so overwhelming that I don’t know what to compare it to,” Tanisha said less than a week after being rushed to the emergency room last spring.

“I almost lost her,” said Manuela Daniels, Tanisha’s mom. “She was in the hospital and the medication was not really working for her. Her heart rate raced up. Her oxygen level dropped real low. It was real bad.”

A GENETIC FLAW

Sickle-cell anemia is a genetic disease, one caused by a defective gene passed from parent to child. Tanisha is one of millions of Americans who will develop some kind of genetic illness during their lifetime. No known treatments or cures exist for most of those diseases.

That could soon change now that scientists have decoded the human genome. A visit to the doctor in the year 2010 might be a very different experience from a visit today.

DNA TESTING

By 2010, DNA tests will be a regular part of any medical exam, according to Francis Collins of the National Human Genome Research Institute. Such tests will examine a patient’s genome for defective genes that cause genetic illnesses.

DNA tests will work like early-warning systems. Say your DNA test reveals that you have a gene for heart disease. Your doctor might then advise you to adopt a more healthful diet and a regular exercise program.

Your doctor might also suggest a new drug to help forestall the development of heart disease. Here again, a DNA test would be ordered, this one to help the doctor know how you will react to the drug.

People vary in the ways they respond to medication. For example, some children produce too little of a certain protein that processes a drug used to treat childhood leukemia. (Leukemia is a life-threatening disease marked by an abnormal increase in white cells in the blood.) If a doctor gives the standard dose of that drug to a child without enough protein to process it, the drug can be deadly. A DNA test can now tell doctors which children produce too little of the protein.

In the future, DNA tests could be available for a wide variety of other drugs. The practice of predicting responses to drug therapy from the results of DNA tests is called pharmacogenetics.

GENE THERAPY

After prescribing a drug that best suits your genetic makeup, your doctor might also suggest gene therapy–replacing bad genes with good ones. In the year 2000, gene therapy is a promising, but still experimental, medical tool.

One of the stumbling blocks to effective gene therapy has been developing tough enough vectors. Vectors are vehicles, such as viruses, that can be used to insert healthy genes into human patients. In experimental trials, doctors have injected good genes into viruses, then injected those viruses into human beings. In most cases, the viruses set off the human immune system, which attacked and destroyed the good genes.

In spite of such setbacks, doctors such as Ken McClain are extremely optimistic about the future of genomic medicine. McClain is an associate professor of pediatrics at Baylor College of Medicine in Houston, Texas. One of McClain’s patients is Tanisha Daniels. McClain predicts that new drug therapies for sickle-cell anemia will soon arise. One day, fetuses with sickle cell anemia may be treated with gene therapy inside the womb. Then sickle-cell anemia will vanish. “That’s the dream,” he said.