How Injured Racehorses Might Save Your Knees


Tendon repair: These ultrasound images show the tendon in a horse’s front leg. An area of damage (circle in yellow, top) has healed (bottom) after the injection of stem cells derived from the animal’s fat.      Credit: Vet-Stem

Orthopedic stem-cell therapies are moving into human trials.

MIT Technology Review, July 20, 2009, by Emily Singer  —  A runner with a torn tendon has reason to envy a racehorse with the same affliction: horses have treatment options not available to human patients–most notably, injections of adult stem cells that appear to spur healing in these animals with shorter recovery time than surgical treatments. Now the same stem-cell therapies used routinely in competitive horses and increasingly in dogs are beginning to make their way into human testing.

Human stem-cell treatments are advancing quickly in many areas: therapies using adult stem cells derived from both fat and bone marrow are currently being tested for a variety of ailments, including Crohn’s disease, heart disease, and diabetes. (Bone-marrow-derived stem-cell transplants have been used for decades to treat blood diseases and some cancers.) But when it comes to orthopedic injuries, such as torn tendons, fractures, and degenerating cartilage, veterinary medicine has outpaced human care.

Veterinarians and private companies have aggressively tested new treatments for the most common injuries in racehorses, in large part because these animals are so valuable and can be so severely incapacitated by these wounds. “Soft-tissue injury is the number-one injury competitive horses will suffer and can end a thoroughbred horse’s career,” says Sean Owens, a veterinarian and director of the Regenerative Medicine Laboratory, at the University of California, Davis. Veterinary medicine also has much more lax regulations when it comes to treating animals with experimental therapies, allowing these treatments to move rapidly into routine clinical use without clinical trials. “Regulatory oversight of veterinary medicine is minimal,” says Owens. “For the most part, the USDA [U.S. Department of Agriculture] and the FDA [Food and Drug Administration] have not waded into the regulatory arena for us.”

Owens’s newly created research center aims to move both animal and human stem-cell medicine forward by conducting well-controlled trials not often performed elsewhere. “Part of our mission is to do basic science and clinical trials and also improve ways of processing cells,” says Owens. The center has a number of ongoing clinical trials in horses–one for tendon tears and one for fractured bone chips in the knee–that are run in a similar way to human clinical trials. The goal is to develop better treatments for horses, as well as to leverage the results to support human studies of the same treatments. Owens is partnering with Jan Nolta,director of the Stem Cell Program, at UC Davis, who will ultimately oversee human testing.

A handful of studies in animals have shown that these stem-cell therapies are effective, allowing more animals to return to racing, reducing reinjury rates, and cutting healing times. VetCell, a company based in the United Kingdom that derives stem cells from bone marrow, has used its therapy on approximately 1,700 horses to date. In a study of 170 jumping horses tracked through both treatment and rehabilitation, researchers found that nearly 80 percent of them could return to racing, compared with previously published data showing that about 30 percent of horses given traditional therapies could return to racing. After three years, the reinjury rate was much lower in stem-cell-treated animals–about 23 percent compared with the published average of 56 percent, says David Mountford, a veterinary surgeon and chief operating officer at VetCell.

While scientists still don’t know exactly how the cells aid repair of the different types of injuries, for tendon tears, initial studies show that stem cells appear to help the tissue regenerate without forming scar tissue.

Mountford says that the company chose to focus on tendon injuries in horses in part because they so closely resemble injuries in humans, such as damage to the Achilles tendon and rotator cuff. For both people and horses, tendon tears trigger the formation of scar tissue, which has much less tensile strength and elasticity than a healthy tendon. “It becomes a weak spot and prone to injury,” says Owens.

Next year, VetCell plans to start a human clinical trial of its stem-cell treatment for patients with degeneration or damage of the fibers of the Achilles tendon. As in the horse therapy, stem cells will be isolated from a sample of the patient’s bone marrow, then cultured and resuspended in a growth medium also derived from the patient. Surgeons will then inject the solution into the area of damage, using ultrasound imaging to guide the needle to the correct location. “Our long-term goal is to use it to treat a number of tendon injuries,” says Mountford.

Stem-cell therapies also show promise for arthritis. Vet-Stem, a California-based company that uses stem cells isolated from fat rather than bone marrow, has shown in a placebo-controlled trial that the treatment can help arthritic dogs. “About 200,000 hip replacements are done every year in humans,” says Robert Harman, a veterinarian and founder of the company. “That’s a very good target for someone to look at cell therapy.”

For osteoarthritis, the stem cells seem to work not by regenerating the joint, but by reducing inflammation. “But in the last couple of years, evidence has come out that the cells we use reduce inflammation and pain, and help lubricate the joint,” says Harman.

While Vet-Stem does not plan to move into human testing, Cytori, a company based in San Diego, has developed a device for isolating stem cells from fat in the operating room. (Vet-Stem does the procedure manually: veterinarians collect a fat sample from the animal and then send it to the company for processing.) Cytori’s device is currently approved for use for reconstructive surgeries in Japan but not yet in the United States.


Caspar the Fish: By creating a transparent zebrafish, Harvard researcher Leonard Zon could watch fluorescently labeled hematopoietic stem cells from a donor fish repopulate the bone marrow of the recipient. The transparent mutant zebrafish, dubbed Caspar, provided a means for studying the effects of FT1050, an experimental drug now in clinical trials to boost the effectiveness of cord-blood transplants.
Credit: Cell Stem Cell
A startup aims to spur the body’s native stem cells to heal disease.

MIT Technology Review, July 20, 2009, by Lauren Gravitz  —  Fate Therapeutics, a startup based in La Jolla, CA, aims to harness the body’s ability to heal itself by developing drugs that stimulate resident stem cells. Rather than developing cell transplants to replace diseased or damaged tissue, which is the focus of a great deal of stem-cell research, Fate is searching for molecules that can control the behavior of adult stem cells in different parts of the body. The two-year-old company began its first clinical trial in May of a novel molecule that could make cord-blood transplants more effective by enhancing the activity of the stem cells that create the blood and the immune system.

The human body is full of adult stem cells–small populations of tissue-specific stem cells that are capable only of developing into the cells of their resident tissue, and whose job is to help maintain and repair that tissue. While they lack the flexible fate of embryo-derived stem cells, adult stem cells come in a variety of flavors, including those capable of making liver cells and immune and blood cells, among others. Fate Therapeutics believes that, with a little pharmaceutical prompting, these cells can be nudged to repair tissue and organ systems, or even fight back against cancer.

“[Adult stem cells] can be induced to proliferate, they can be induced to differentiate into the cell type they were destined to become, or potentially even induced to become something they weren’t destined for that might be therapeutically relevant,” says Paul Grayson, Fate’s president and CEO.

To better understand how to activate and command adult stem cells, Fate has focused much of its research on induced pluripotent stem (iPS) cells, adult cells that have been reprogrammed back to an embryonic state and have the same flexible developmental potential as embryonic stem cells. Rather than trying to use these iPS cells to treat disease, Fate is using them as a discovery tool to learn more about which pathways are important for activating or inhibiting stem-cell development.

“Fate’s strategy is to try and take advantage of what we’re learning about stem-cell biology to develop methods of using drugs to turn on or turn off stem cells,” says David Scadden, one of the company’s founders and director of the Center for Regenerative Medicine at Massachusetts General Hospital. Scadden and other top investigators from regenerative-medicine institutes across the country–including MIT, Scripps, and Stanford–were brought together by a group of venture capitalists who saw Fate Therapeutics as a way to quickly take their research to the forefront of stem-cell science.

Fate has raised $25 million in capital and is backed by three venture-capital groups. The company has been building its intellectual-property portfolio by licensing technology from different universities, focusing in part on iPS cell technology, as well as patenting the stem-cell discoveries of its founders and in-house scientists.

Fate’s first clinical trial focuses on a molecule known as FT1050. The molecule appears to stimulate proliferation of hematopoietic stem cells–which give rise to blood and immune cells–and helps guide them to the bone marrow. If successful, the drug could become an invaluable companion treatment to bone-marrow transplants and cord-blood transfusions used to treat cancer and blood diseases.

Treatment for leukemia or lymphoma, for example, kills off most of a patient’s hematopoietic stem cells, and the best way to repopulate them is through bone marrow transplanted from a matched donor. When a bone-marrow donor match is unavailable, oncologists turn to umbilical-cord blood, which is rich in stem cells and requires only a partial tissue-type match. However, cord blood is also incredibly expensive, costing upwards of $30,000 or more per unit, and blood from a single cord is often insufficient to treat an adult.

“It becomes very difficult to find a unit large enough to sufficiently large enough for a full-grown adult,” says Dennis Confer, chief medical officer of the National Marrow Donor Program. Physicians can sometimes use blood from two cords, but this is even more expensive and requires that both cord samples match the donor. “If someone could come up with an expansion strategy that was more cost-effective, that could gain wide acceptance,” he says.

In an early-stage clinical trial, Fate Therapeutics is testing FT1050 in 12 patients who’ve undergone chemotherapy for lymphoma. The patients will each receive two units of cord blood: one that’s been treated with the stem-cell-modulating drug, and another that’s been left alone. The trial is primarily a safety study, but because the two units were harvested from two different newborns, researchers can use the genetic differences to track the cells and determine if FT1050-treated stem cells can more efficiently take hold and prosper in bone marrow.

Fate believes that multiple conditions can be treated this way, using small molecules to control adult stem-cell activity. The company is even pursuing the same strategy for cancer treatments, with the hope that they can disrupt the uncontrolled growth of cancer cells by forcing them into a more differentiated, less malignant state.


Rapamycin, an immunosuppressant, enables elderly mice to live longer.

MIT Technology Review, July 20, 2009, by Jocelyn Rice  —  A drug derived from bacteria in the soil on Easter Island can substantially extend the life span of mice, according to a study published online today in Nature. The drug, called rapamycin, is the first pharmacological agent shown to enhance longevity in a mammal, and it works when administered beginning late in life. Prior to this research, the only ways to increase rodents’ life span were via genetic engineering or caloric restriction–a nutritionally complete but very low-calorie diet.

Rapamycin is an antifungal compound already approved by the FDA as an immunosuppressive therapy to help prevent organ rejection in transplant patients. It is currently being tested in clinical trials for potential anticancer effects.

The drug had previously been shown to extend life span in invertebrates. “[This study is] exciting because it shows that it’s feasible to do this in a mammal,” says David Sinclair, codirector of the Paul F. Glenn Laboratories for the Biological Mechanisms of Aging at Harvard Medical School, who was not involved in the study. “Maybe 20 years from now we’ll look back at this study as a landmark that pointed the way to medicines of the future.”

In the new study, researchers found that rapamycin given to mice as a food supplement starting at 20 months of age–the equivalent of 60 years in humans–extended average life span by 9 percent in males and 13 percent in females. “It’s particularly exciting because it works so late in life to extend life span,” says Sinclair. “The fact that you can give a drug after 20 months of age in a mouse and still see a life-span extension is striking.”

The results were pooled from three independent studies–at Jackson Laboratory, in Bar Harbor, ME; the University of Texas Health Science Center, in San Antonio; and the University of Michigan, in Ann Arbor–and coordinated by the National Institute of Aging’s Interventions Testing Program (ITP). Rapamycin is the first success story to emerge from the ITP, which systematically evaluates anti-aging drug candidates for effectiveness in mice.

Experts believe it’s possible that rapamycin may tap into one of the same biochemical pathways as calorie restriction, an intervention long known to make mice live longer. While the drug was not as effective as a limited diet initiated early in life, it was far more powerful than a limited diet begun at the same advanced age. In ongoing studies, the researchers are testing different doses across a range of starting ages; an optimal combination may ultimately prove more potent than calorie restriction.

Stumbling across rapamycin’s late-in-life efficacy was a happy accident. Originally, the therapy was to begin at four months of age, but the amount of rapamycin required to sustain therapeutic blood levels turned out to be prohibitively expensive. By the time the researchers devised a solution–microencapsulating the drug in a polymer coating that only disintegrates in the intestine–the mice were much older.

The research team decided to go ahead with the study anyway, because if there was an effect with late-in-life administration, it would be particularly relevant for humans. Initiating a human treatment early in life would be less practical, and would expose patients to side effects for longer, says David Harrison, principal investigator of the Jackson Laboratory portion of the study. (Because the drug suppresses the immune system, patients taking it are more susceptible to dangerous infections.)

Besides targeting older animals, the study is also unusual for its use of a genetically diverse population of mice. Most aging studies use inbred strains, which are easier to work with in the laboratory. Harrison says that a genetically heterogeneous study population rules out the possibility of accidentally treating a specific disease that happens to be prevalent in the inbred strain being used. Much like humans, the mice used in the study have a wide variety of susceptibility to the various diseases of aging. Since the life-span-extending effects were seen throughout the study population, says Harrison, rapamycin must be altering some fundamental aging mechanism that drives a broad range of age-related defects.

“People who study the biology of aging feel that in order to deal with diseases of aging, it’s much more efficient to target underlying mechanisms, rather than focusing on heart disease or cancer or diabetes or Alzheimer’s or Parkinson’s separately,” says Harrison. “If we could alter underlying mechanisms of aging, all of these things would be postponed.”

Exactly what rapamycin’s mechanism might be remains to be seen, says Harrison. The drug inhibits a protein called target of rapamycin (TOR). Normally, TOR helps cells manufacture new proteins, and hinders the destruction of malfunctioning ones. While these processes are known to be involved in aging in fruit flies, nematode worms, and yeast, TOR’s precise role in life-span regulation is still unclear.

It’s promising to learn that TOR also participates in mouse aging, because it means that the mechanism is relevant in all four model organisms most widely used to study the aging process, says Matt Kaeberlein, a professor of pathology at the University of Washington and coauthor of a commentary accompanying the new study. “The fact that it’s been conserved over that large evolutionary distance makes it an intriguing possibility that TOR signaling has similar effects in people,” he says.

Teasing out precisely how TOR signaling is linked to life span could reveal new targets for potential anti-aging drugs. By zeroing in on a different part of the TOR pathway, future drugs may be able to avoid some of rapamycin’s troubling side effects.

The authors caution that it’s still not clear whether rapamycin will have similar life-span-enhancing effects in humans, and that because of its known toxicities, such as fungal infections and pneumonia, the drug should not be taken by the general population as a kind of universal fountain of youth.

A more realistic goal, says Kaeberlein, is to investigate whether it can treat specific age-related disorders–as in the several ongoing cancer trials, for example. Studies have also suggested that interfering with the TOR signaling pathway could slow the progression of Huntington’s disease, Alzheimer’s disease, and diabetes. “Realistically,” says Kaeberlein, “I think what most of us are hoping for, and are somewhat optimistic about, is the idea that you may be able to get an extra decade–possibly an extra two decades–of relatively good health.”


Squeezing Your Way to Lower Blood Pressure


A simple hand exercise could help you lower your blood pressure without drugs.

A hand grip designed to keep fighter pilots from blacking out during sharp turns and steep dives has an interesting therapeutic benefit on the ground – lowering blood pressure without medication.

Squeezing the grip for a few minutes a day has been shown to lower blood pressure as much as a first-line antihypertension drug. How it does this is still something of a medical mystery.

From air to earth

In the mid-1970s, the U.S. Air Force asked Dr. Ronald Wiley, an expert in heart and lung physiology, to find a way to keep fighter pilots from losing consciousness when flying the F-16 fighter. This jet could accelerate so fast that the G-forces it generated made it difficult for the pilot’s heart to pump blood to the brain, causing vision problems, trouble thinking, and blackouts.

One of Wiley’s strategies was a hand grip that pilots could squeeze to boost their blood pressure enough to maintain circulation to the brain. As he worked with pilots, he was struck by a contradiction – those who practiced with the hand grip for a few weeks lowered their resting blood pressure.

After several years of tinkering, Wiley refined the hand grip to minimize the blood pressure spike caused by isometric muscle contractions. The first version was a boxy machine called the CardioGrip. Today’s sleeker one is being sold as the Zona Plus.

The Zona Plus looks like an electric razor. You hold it in your right hand and squeeze as hard as you can for five seconds. The device measures the strength of your squeeze and calculates a target 30% as strong. You do the same thing with your left hand.

The device then prompts you through four 2-minute bouts of squeezing, with a minute break between each one. You squeeze just hard enough to keep the “Hold” sign in the display atop the hand grip (see photo). A beep and a visual signal tell you if you are squeezing too hard or not hard enough.

The whole session, which should be done at least three times a week, lasts about 12 minutes. You can do it while watching the news, reading a book, or any other time you are sitting still for a few minutes.

Modest reductions

A handful of studies have looked at how the CardioGrip and Zona Plus influence blood pressure. All of the studies have been small (under a dozen participants in each) and short (2-3 months). The results, though, have been remarkably similar.

In the eight published studies we reviewed, participants’ systolic blood pressure (the top number of a blood pressure reading) dropped an average of 14 points. The device had little effect on diastolic pressure. As is the case for almost everything in medicine, different people respond differently to the hand grip exercise. Individual responses to using the device for a month or so vary from a 55 mm Hg drop in systolic pressure to the rare but small increase.

If these results hold up in longer, larger studies, they suggest that this simple exercise could lower blood pressure as much as a first-line antihypertension drug. And it’s conceivable that use of the Zona Plus could help people with normal blood pressure avoid the gradual creep upward that usually comes with age.

Researchers haven’t yet figured out how an exercise involving only the forearm lowers blood pressure. Neil McCartney, who chairs the kinesiology department at McMaster University in Ottawa, Canada, and his colleagues have done several studies on the Zona Plus. He suspects that moderate-level isometric training somehow helps the body turn down activity of the sympathetic nervous system, which increases heart rate and blood pressure, and turn up the vagal system, which has a calming effect.

Exercise addition, not replacement

The Zona Plus doesn’t offer an immediate fix for high blood pressure. You have to use it for four to six weeks to see any results. It isn’t a cure for high blood pressure, since if you stop doing the exercise your blood pressure will begin to creep back up. And it isn’t a substitute for regular aerobic exercise. While it may lower your blood pressure, you still need brisk walking, swimming, bicycling, or other activities to strengthen your heart, blood vessels, lungs, and bones, and to keep your blood sugar under control. Most people can use the Zona Plus; the company that makes the device says it isn’t for people with arthritis in the hands, carpal tunnel syndrome, nerve damage from diabetes, an aneurysm, or mitral valve problems.

Although the Zona Plus is FDA approved, it isn’t yet covered by Medicare or most large health insurers. At $300, it represents a substantial out-of-pocket expense. That may be money well spent, though, if it keeps your blood pressure under control or lets you eliminate a blood pressure drug from your daily handful of pills. As an added incentive, the Zona Plus comes with a money-back guarantee if you don’t see an improvement in your blood pressure after using it as directed for eight weeks.

For more information about the Zona Plus, call 866-669-9662 (toll free) or visit

MIT Technology Review, July 20, 2009, by Emily Singer  —  As direct-to-consumer genetic testing spreads, a major concern expressed by ethicists and physicians has been whether the average person will be able to understand the results of these somewhat subtle tests. Rather than giving an answer in black and white, the tests predict whether someone has an elevated risk for developing common diseases, such as Alzheimer’s. Even if consumers do understand the results, it has been unknown how they might react to news that they have a sequence of DNA that raises their risk of developing a disease.

Two new studies suggest that most patients cope easily with such negative genetic information. People who learn that they carry a high-risk genetic variant for Alzheimer’s disease, called APOE4, have no greater anxiety over their long-term prospects than do those who don’t know their risk, according to research published in the New England Journal of Medicine. Another recent study of smokers revealed that those who found out that they had a lower genetic risk for developing lung cancer were just as interested in stopping smoking as those determined to be at higher cancer risk.

“The findings may help us to subdue paternalistic concerns that we have to protect people from this information,” says Colleen McBride, chief of the Social and Behavioral Research Branch at the National Human Genome Research Institute, in Bethesda, MD, and senior author on the smoking study. “People given the option to take these tests can protect themselves, and they find it useful to know the results, even if the test hasn’t been proven to make a difference in what they do.”

In the past few years, a number of companies have sprung up to offer genetic testing directly to consumers. “Studies like this are important because we are clearly going to see testing like this make its way routinely into mainstream medicine,” says Michael Christman, president of the Coriell Institute for Medical Research. Because the results of this type of testing are much more complex than the genetic tests currently used most commonly in medicine–largely single-gene testing for rare, severe disorders, such as cystic fibrosis–physicians worry about how people will react. Some have speculated that someone at high risk for neurological disease might give up on long-term relationships, or someone at low genetic risk for type 2 diabetes might indulge in a diet of doughnuts and cheeseburgers.

To date, most sociological studies of genetic testing have focused on rare inherited diseases rather than on more common ones, such as Alzheimer’s. Robert Green and his colleagues at Boston University are among just a handful of researchers examining this issue: Green’s team has spent the past decade studying the impact of genetic testing for APOE4, which raises the risk of developing Alzheimer’s disease threefold in those who inherit one copy and tenfold in those who have two copies. No proven treatments exist to reduce Alzheimer’s risk in APOE4 carriers, and testing for the risk variant is not currently recommended. But surveys indicate that 15 percent of primary-care physicians who treat patients with Alzheimer’s have already been asked about the test.

In the newly published study, Green and his colleagues offered APOE4 testing to adult children of people with Alzheimer’s disease and then revealed the results to half of the group. The team found that people clearly understood their results, and that six weeks after learning them, those who were told that they had the high-risk variant seemed more stressed than the other participants. But that spike in anxiety had faded by the time participants were tested again both six months and one year afterward.

“We were astounded by how many people wanted to know.  More than 20 percent wanted to receive it,” says Green. “Even though patients clearly understood there was nothing they could do to stave off the disease, they had nonmedical reasons to learn about it: to prepare their children, to think about the longevity of careers.”

For example, “people do in fact change insurance purchasing behavior based on this information,” says Green. “We should be cautious as medical professionals not to dismiss those personal reasons, as long as we can convince ourselves it’s not harmful to offer this information.”

Green and his collaborators have also found that people who know they have the high-risk gene are more likely to take vitamins. “That’s fine, except that some types of supplements are highly unregulated and can be harmful,” he says. “You can easily imagine people trying to link results of genetic tests to the purchase of unproven vitamins that could at best take their money and distract them, and at worst could be harmful.”

Researchers caution that results from the study are not necessarily indicative of the general population. For example, Green’s team weeded out people who scored high on measures of anxiety and depression at the start of the study. And the study does not examine all of the potential drawbacks of testing. In an editorial accompanying the paper, Rosalie Kane, a public-health specialist, and Robert Kane, a physician, both from the University of Minnesota, in Minneapolis, say that people who test positive for high-risk genetic variants might be denied some types of insurance. The Genetic Non-Discrimination Act, passed last year, prohibits such discrimination in employment and health insurance, but not in life, disability, or long-term care insurance.

One of the other major concerns for the new generation of genetic testing is how best to deliver the results. In Green’s APOE4 study, participants learned of their risk through genetic counselors–but this may not always be possible as genetic testing becomes more widespread. “I would be interested going forward to see how people who received this information without counseling deal with it,” says Christman. “Some of the direct-to-consumer companies are doing this right now.”

In the lung-cancer study, McBride and her collaborators offered smokers who had a family member with lung cancer genetic screening for a variant associated with a higher risk of developing lung cancer. Information about the risks and benefits of the test, provided to help people decide whether to take it, as well as the results were delivered online.

The researchers found that all of the people in the study who tested high risk understood the meaning of the results, while only about 60 percent of those who scored low risk understood them. “That kind of defies expectation,” says McBride. “Psychological theories predict that people protect themselves from threatening information, and one way to do that is by not understanding it.”

The researchers found no difference between the high- and low-risk participants’ interest in getting additional tools to quit smoking. “Telling someone they are low risk doesn’t undermine their motivation to seek out cessation materials, and being told you are high risk didn’t increase motivation,” McBride says. “All smokers were motivated enough to log on and consider testing and availed themselves of cessation materials.”

McBride says that she doesn’t think genetic testing itself will motivate people to quit smoking or lose weight or make whatever changes might help their health. Instead, she says that the tests’ utility may be to motivate people to take initial steps–“to get someone engaged in a smoking-cessation program or dietary-change intervention.”

McBride is now studying the impact of genetic tests that analyze many spots on the genome and assess risk for multiple diseases, such as those offered by a number of online gene-testing companies. “There the story is much more complicated,” she says. “The results might conflict with each other, and people might be at risk for many conditions.”

20090721-4, July 20, 2009, by Kristin Channas  —  July may be the time for lemonade, fireworks and fun in the sun, but weather watchers warn of a less positive distinction:

“July typically is the month with the greatest number of lightning fatalities,” said John Jensenius, the lightning expert for the National Weather Service. “We tend to see the fatalities come in somewhat randomly.”

So far this month, lightning has caused seven U.S. deaths, all of which occurred in the first eight days of July. The 30-year-average for July is 17 deaths, he said. This year, there have been 23 deaths nationally:  two in Texas and California, four in Florida, and the remainder occurring in 14 other states, with one in Puerto Rico.

“At this point, Florida had more fatalities than anywhere else with four,” he said.  Areas around Colorado and New England also experience a lot of lightning during the summer months.

The season continues through July and August, with fatalities increasing as people spend more time outside.  “It can strike during recreational activities like boating, sometimes jogging or baseball, or while performing day-to-day chores like cutting the lawn or taking out the trash,” he said.

Lightning can even strike in seemingly clear skies. “It’s called a bolt from the blue,” says Dr. Corene Matyas, assistant professor of geography at the University of Florida.  “There are no clouds overhead. It may have never even rained where you are, but lightning can still strike.”

Bolts of lightning can travel horizontally and strike 10 miles from a thunderstorm before making contact with the ground. “You don’t have to be directly underneath the cloud to get struck by lightning,” Matyas said.

“A bolt of lightning is more than five times hotter than the sun,” said Matyas, noting that the energy spreads as soon as it makes contact with the ground. “If it hits water, a very good conductor, it can travel quickly to a great distance.”

Jensenius offered the following safety tips:

-Have a lightning safety plan. “The main thing for people to realize is if you hear thunder, lightning is in striking distance,” he said. “Plan ahead so you avoid thunderstorms.”

-Postpone activities like boating to avoid being caught in a dangerous situation.

-Monitor the weather. Darkening skies, flashes of lightning or increased wind are all signs of a developing thunderstorm.

-Get to a safe place. Fully enclosed buildings with wiring and plumbing provide the best protection. Picnic shelters do not protect you from lightning. If a sturdy building is not nearby, get into a hard-topped metal vehicle and close all the windows. Stay inside until 30 minutes after the last rumble of thunder.

-If you hear thunder, don’t use a corded phone except in an emergency. Cordless phones and cell phones are safe to use.

-Keep away from electrical equipment and wiring.

-Water pipes conduct electricity. Don’t take a bath or shower or use other plumbing during a storm.

“The key is simply there’s no safe place outside during a thunderstorm,” he said. “Plan ahead so you avoid thunderstorms altogether.”



New Study Sheds Light on the Growing U.S. Wind Power Market

For the fourth consecutive year, the U.S. was home to the fastest-growing wind power market in the world in 2008, according to a report released by the U.S. Department of Energy and prepared by Lawrence Berkeley National Laboratory (Berkeley Lab). Specifically, U.S. wind power capacity additions increased by 60 percent in 2008, representing a $16 billion investment in new wind projects. “At this pace, wind is on a path to becoming a significant contributor to the U.S. power mix,” notes report author Ryan Wiser, of Berkeley Lab. Wind projects accounted for 42% of all new electric generating capacity added in the U.S. in 2008, and wind now delivers nearly 2% of the nation’s electricity supply.


The 2008 edition of the “Wind Technologies Market Report” provides a comprehensive overview of developments in the rapidly evolving U.S. wind power market. The need for such a report has become apparent in the past few years, as the wind power industry has entered an era of unprecedented growth, both globally and in the United States. At the same time, the last year has been one of upheaval, with the global financial crisis impacting near-term growth prospects for the wind industry, and with federal policy changes enacted to push the industry towards continued aggressive expansion. “With the market evolving at such a rapid pace, keeping up with trends in the marketplace has become increasingly difficult,” notes report co-author Mark Bolinger. “Yet, the need for timely, objective information on the industry and its progress has never been greater…this report seeks to fill that need.”


Drawing from a variety of sources, this report analyzes trends in wind power capacity growth, turbine size, turbine prices, installed project costs, project performance, wind power prices, and how wind prices compare to the price of conventional generation. It also describes developer consolidation trends, current ownership and financing structures, and trends among major wind power purchasers. Finally, the report examines other factors impacting the domestic wind power market, including grid integration, transmission issues, and policy drivers. The report concludes with a preview of possible near- to medium-term market developments.


Some of the key findings from the just-released 2008 edition include:


  * *The U.S. is the fastest-growing wind market worldwide*. The U.S.

    has led the world in new wind capacity for four straight years,

    and overtook Germany to take the lead in cumulative wind capacity


  * *Growth is distributed across much of the U.S.* Texas leads the

    nation with 7,118 MW of new wind capacity, but 13 states had more

    than 500 MW of wind capacity as of the end of 2008, with seven

    topping 1,000 MW, and three topping 2,000 MW. Over 10% of the

    electricity generation in Iowa and Minnesota now comes from wind


  * *Market growth is spurring manufacturing investments in the U.S.*

    Several major foreign wind turbine manufacturers either opened or

    announced new U.S. wind turbine manufacturing plants in 2008.

    Likewise, new and existing U.S.-based manufacturers either

    initiated or scaled-up production. The number of utility-scale

    wind turbine manufacturers assembling turbines in the U.S.

    increased from just one in 2004 (GE) to five in 2008 (GE, Gamesa,

    Clipper, Acciona, CTC/DeWind).

  * *Wind turbine prices and installed project costs continued to

    increase into 2008*. Near the end of 2008 and into 2009, however,

    turbine prices have weakened in response to reduced demand for

    wind due to the financial crisis.

  * *Wind project performance has improved over time, but has leveled

    off in recent years.* The longer-term improvement in project

    performance has been driven in part by taller towers and larger

    rotors, enhanced project siting, and technological advancements.

  * *Wind remained economically competitive in 2008. *Despite rising

    project costs, in recent years wind has consistently been priced

    at or below the price of conventional electricity, as reflected in

    wholesale power prices. With wholesale prices plummeting in recent

    months, however, the economic position of wind in the near-term

    has become more challenging.

  * *Expectations are for a slower year in 2009, in large part due to

    the global recession.* Projections among industry prognosticators

    range from 4,400 MW to 6,800 MW of wind likely to be installed in

    the U.S. in 2009. After a slower 2009, most predictions show

    market resurgence in 2010 and continuing for the immediate future.

Berkeley Lab’s contributions to this report were funded by the Wind & Hydropower Technologies Program, Office of Energy Efficiency and Renewable Energy of the U.S. Department of Energy.
Berkeley Lab is a U.S. Department of Energy national laboratory located in Berkeley, California. It conducts unclassified scientific research for DOE’s Office of Science and is managed by the University of California. Visit our website at <>.
*Additional Information:*– The report, “2008 Wind Technologies Market Report”, can be downloaded from:
– A PowerPoint presentation summarizing key findings from the report can be found at:
– The Department of Energy’s press release is available at: <http://>