You Can Get A Watch

SEQUOIA AND KINGS CANYON NATIONAL PARKS, Calif. — From the summit of Bishop Pass in the Sierra Nevada, elevation 11,972 feet, all you can see are miles of granite peaks against the sky. There is no traffic and no pollution. The natural world seems pure and unspoiled.
But appearances are deceiving. Over the last decade, disaster has struck in the form of chytridiomycosis, or chytrid, a deadly fungal disease that has driven at least 200 of the world’s 6,700 amphibian species to extinction. One third of the world’s frogs, toads and salamanders are threatened. Forty percent are declining. Chytrid’s arrival has laid waste to the indigenous Sierra Nevada yellow-legged frog, Rana sierrae.

In Dusy Basin, a remote glacial valley in Sequoia and Kings Canyon National Parks a few miles west of Bishop Pass, Vance Vredenburg, a professor of biology at San Francisco State University, is conducting an experiment he hopes will help preserve what remains of these once abundant creatures. Dr. Vredenburg and his colleagues are inoculating chytrid-infected frogs with a bacteria, Janthinobacterium lividum, or J. liv, that does not prevent infection with chytrid but can help frogs survive.

Dr. Vredenburg, Reid Harris of James Madison University in Harrisonburg, Va., and colleagues found the symbiotic bacteria on several amphibian species. Lab experiments last year showed that J. liv produces a metabolite, violacein, that is toxic to the chytrid fungus. Dr. Vredenburg wants to see how effective the treatment will be in the wild.

Even before chytrid arrived, the Sierra frog population had been severely reduced by the California Department of Fish and Game’s practice of seeding high-elevation lakes with hatchery-raised fingerling trout for the sport fishing industry. Chytrid has hastened the destruction. Dr. Vredenburg and colleagues counted 512 populations scattered among the thousands of mountain lakes in the park in 1997. In 2009, 214 of these populations had gone extinct. A further 22 showed evidence of the disease. It is a far cry from the early 1900s, when frogs in the region were so common that lakeside visitors reported trampling them underfoot.

Dr. Vredenburg, 41, has been doing frog research in the Sierra since the mid-1990s. He chose frogs as research subjects because he wanted to do “basic science that could be applied toward solving some real-world problems, like the biodiversity crisis. Once your study animals start dying, believe me, you pay attention!” At the time, he said, “I saw many scientists as living and working in a bubble. Besides,” he added, “I like catching frogs.”

For his Ph.D. at the University of California, Berkeley, under the mentorship of David Wake, Dr. Vredenburg measured the effects introduced trout were having on mountain yellow-legged frog populations. The results were clear: They wreaked havoc. Brown and rainbow trout, not native at higher elevations, are voracious consumers of tadpoles. In 2001, as a result of work by Dr. Vredenburg and Roland Knapp of the Sierra Nevada Aquatic Research Laboratory, the state fish and game agency and the National Park Service began a gill netting project to remove them. In areas where trout were removed, frogs recovered.

Curtis Milliron, a senior biologist at the fish and game department, pointed out that historically the agency has played a dual, sometimes paradoxical role. “We’re both ecological stewards and recreational purveyors,” Mr. Milliron said. Although his agency is implicated in frog decline, now his charter is to create “a biodiversity management plan where we can maintain frog habitat and implement frog recovery.”

Leaders at the National Park Service, too, once felt that “we need to protect the national parks from research scientists,” said David Graber, chief scientist for the service’s Pacific West region. Scientists’ agendas were viewed as being at odds with the service’s mandate, which calls for conservation and preservation as well as making parks available for recreation. “Now it’s different,” Dr. Graber said. “Now all we care about are the massive frog die-offs. We’re passionate about conservation. We can’t wait for ‘survival of the fittest.’ ”

Dr. Vredenburg himself was “speechless” when the park service granted permission to carry out the J. liv experiment in Dusy Basin. “Then I had to start planning,” he said.

Dr. Vredenburg chose Dusy Basin for his experiment because chytrid is just arriving here. Unlike Sixty Lake Basin several miles to the south, where frogs went extinct within four years of the arrival of chytrid, Dusy Basin still has frogs. Biologists do not know what first brought chytrid to the Sierra. But Dr. Vredenburg’s research showed that chytrid spreads in a linear wave across the landscape, an infection pattern like that of human epidemics. Infection levels start out light, then increase to very high. Then there is a mass die-off.

In July, Dr. Vredenburg and his students captured and tagged 100 frogs, apparently the last remaining here, with transponder tags. They weighed and measured frogs, and they recorded the tag numbers using an electronic reader. The experimental group contained 80 frogs; 20 were designated controls. Dr. Vredenburg and his students placed experimental frogs in plastic containers for an hourlong bath in cultured J. liv — long enough for J. liv to colonize on frogs’ skins. They released the frogs into the ponds and streams where they had been captured.

We've all seen the commercials. There's a sad little white marshmallow, a person in a darkened room unable to attend the party, or unable to enjoy a beautiful day. And then a voice shouts out that here is hope. That depression of yours is a result of imbalances in chemicals in your brain and, if you can correct those chemicals, you will feel better. Easy!

It's not that these commercials sell you a pack of lies. Most antidepressants do increase the levels of chemical messengers in the brain called neurotransmitters. A specific type of neurotransmitter, the monoamines, appear to be the chemicals of choice for these drugs. Scientists once thought that simply increasing the amount of monoamines in the brain would treat the symptoms of depression. And that meant, of course, that depression itself must be caused by low levels of monoamines, particularly serotonin.

For years, scientists have tried to find drugs that increase these serotonin levels in the brain safely, and tried to find evidence that decreases in monoamines are responsible for depression itself.

Well, after much searching, we did find a lot of very interesting things. But some things just didn't add up.

The first problem was one of time. If low serotonin levels were really what made you feel depressed, then increasing levels of serotonin should alleviate the symptoms right away. But antidepressants don't work immediately, and in fact can take more than a month to alleviate symptoms. Strike one.

The second problem was one of whether the drugs actually worked. Serotonin-specific antidepressant drugs don't work on everyone. In fact, new estimates show that the current antidepressants on the market only work in about 60% of patients. If low serotonin levels were really responsible for depression, then increasing serotonin should have worked on more than 60% of patients. Strike two.

The final problem is one of evidence. If low serotonin levels were responsible for depressed mood, then we should be able to induce depression in people by decreasing serotonin, and we should find low levels of serotonin in patients with depression. But neither of those things exist. Decreasing serotonin in humans can lower your mood, but it doesn't always work. And studies looking for low serotonin in depressed patients have been inconclusive. It appears that even though antidepressants increase serotonin, a lack of serotonin doesn't cause depression (kind of like aspirin treats a headache, but headaches are not caused by a lack of aspirin). Strike three. Serotonin is out.

So what's in? After all, antidepressants do work in some patients. It's instructive to look at other things these drugs are doing in the brain.

Antidepressants increase levels of neurotransmitters in the brain, but they also increase neurogenesis, the birth of new cells in the brain. Throughout your life, you will grow new neurons in an area of the brain called the hippocampus. And if you take antidepressants for several weeks, you will get increased neurogenesis.

These new neurons correspond to changes in animal behaviours that are associated with long-term antidepressant treatment. The behaviours are novelty-induced hypophagia, which measures how much of a tasty food an animal will eat in a novel environment and reflects aspects of anxiety and anhedonia (the inability to experience pleasure); and the tail suspension test, which measures behavioural despair.

1. The first working laser was built by Theodore Maiman and "fired" at Hughes Research Laboratories, Malibu, California on 16 May 1960.

2. Einstein set the theoretical foundations for the laser more then 30 years earlier in his 1917 paper, The Quantum Theory of Radiation.

3. Putting it very, very simply, you bounce light energy between mirrors at both ends of a tube. One of them is translucent, allowing a beam to pass through.

4. They have featured in hundreds of films, the most famous being the cutting beam heading for James Bond's crotch in Goldfinger; it has spawned imitations from Austin Powers to The Simpsons' Itchy and Scratchy.

5. No need to fear the dentist; beams can remove rot painlessly. Or you could just floss more.

6. The laser printer familiar to anyone who works in an office was invented in 1969 by Xerox, but wasn't commercially available until 1979. Oh, and it took up a whole room.

7. Four years later, LaserDisc – a sort of oversized DVD – marked the first time lasers were used for recording films or music. It never really caught on.

8. The name stands for: Light Amplification by Stimulated Emission of Radiation.

9. One in five British people who get tattoos later regret them. Many turn to laser surgery.

10. They gave us "bloodless" surgery: heat from the beam cuts and cauterises at the same time.

11. The first everyday commercial use of lasers was in supermarket barcode scanners in 1974.

12. But they aren't just for boring stuff. Pink Floyd and The Who pioneered laser light shows. Now no self-respecting band goes on tour without them.

13. On the downside, when you get zapped by a speed cameras, it is a laser that clocks you by bouncing off your car.

14. Laser pointers – loved by lecturers the world over – cost hundreds when they first appeared in shops in the 1980s; now you can pick one up for 50p.

15. Unfortunately, that means hooligans can afford them: in 2008, South Korean goalkeeper Lee Woon-Jae was hit in the eye while playing Saudi Arabia in a World Cup qualifier.

16. Who first invented the term "laser" was the subject of a 28-year patent lawsuit between physicist Gordon Gould and Bell Laboratories.

17. The glowing light sabres used in Star Wars were inspired by laser technology. They are "the most popular film weapon of all time", according to a survey by Twentieth Century Fox.

18. Lidar – using lasers to measure far-off objects – is more accurate than radar. Lucky really, because the ash cloud is back again.

19. Powerful as they were, lasers were dismissed by scientists at first as a "solution looking for a problem".

20. Nevertheless, Apollo 11 astronauts used one to measure the distance from the Earth to the Moon, give or take a finger's width.

21. Using lasers you can get sequencing information about DNA from a single molecule.

22. The first laser eye treatment on a human was done in 1987 by American physician Dr Marguerite McDonald, who described it as being "like a Buck Rogers ray gun".

23. The world's first laser-guided bomb, in 1967, went by the catchy name Bolt-117.

24. Laser measuring is accurate to more than a nanometre (that's a billionth of a metre).

25. In 2004, about 733 million diode lasers, used in DVD and CD players were sold, estimated to be worth about $3.2bn.

drive from www.independent.co.uk